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BACKGROUND: Early adversity, broadly defined as a set of negative exposures during childhood, is extremely common and increases risk for psychopathology across the life span. Previous research suggests that separate dimensions of adversity increase risk through developmental plasticity mechanisms shaping unique neurobiological pathways. Specifically, research suggests that deprivation is associated with deficits in higher order cognition, while threat is associated with atypicality in fear learning and emotion dysregulation. However, most of this research has been conducted in adolescent and adult samples, long after exposure to adversity occurs and far from periods of peak developmental plasticity. OBJECTIVE: The Wellness Health and Life Experiences (WHALE) study examines the neurobiological and behavioral mechanisms by which deprivation, threat, and unpredictability increase risk for psychopathology in early childhood (age 4-7 years) directly following periods of peak developmental plasticity. The objective of this study is to describe the study rationale and aims, the research design and procedures, and the analytical plan to test the study hypotheses. METHODS: This is a retrospective cohort study that examines associations between exposure to deprivation and threat and their hypothesized neurobiological mechanisms, how these neurobiological mechanisms link early adversity and psychopathology, and associations between unpredictability, reward learning, and psychopathology. The sample was a convenience sample of children (aged 4-7 years) and their families, identified through flyers, email blasts to listserves, school-based advertising, and involvement in community events. Data were collected during a home visit, a subsequent laboratory visit, and a final neuroimaging visit. Planned analyses include linear regression, path analyses, and functional magnetic resonance imaging analyses to explore the role of neural function in the association between early adversity and psychopathology. RESULTS: Participants (N=301) have been recruited into the study, and data collection has commenced. The expected results will be available in 2024. CONCLUSIONS: The findings of this study will help elucidate the neurobiological mechanisms by which early adversity increases risk for psychopathology in early childhood. This study represents the earliest test of an influential theory of biological embedding of early adversity. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): DERR1-10.2196/59636.

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Background: Posttraumatic stress disorder and medically unexplained pain frequently co-occur. While pain is common during traumatic events, the processing of pain during trauma and its relation to audiovisual and pain intrusions is poorly understood.Objective: Here we investigate neural activations during painful analogue trauma, focusing on areas that have been related to threat and pain processing, and how they predict intrusion formation. We also examine the moderating role of cumulative lifetime adversity.Methods: Sixty-five healthy women were assessed using functional magnetic resonance imaging. An analogue trauma was induced by an adaptation of the trauma-film paradigm extended by painful electrical stimulation in a 2 (film: aversive, neutral) x 2 (pain: pain, no-pain) design, followed by 7-day audiovisual and pain intrusion assessment using event-based ecological momentary assessment. Intrusions were fitted with Bayesian multilevel regression and a hurdle lognormal distribution.Results: Conjunction analysis confirmed a wide network including anterior insula (AI) and dorsal anterior cingulate cortex (dACC) being active both, during aversive films and pain. Pain resulted in activation in areas amongst posterior insula and deactivation in a network around ventromedial prefrontal cortex (VMPFC). Higher AI and dACC activity during aversive>neutral film predicted greater audiovisual intrusion probability over time and predicted greater audiovisual intrusion frequency particularly for participants with high lifetime adversity. Lower AI, dACC, hippocampus, and VMPFC activity during pain>no-pain predicted greater pain intrusion probability particularly for participants with high lifetime adversity. Weak regulatory VMPFC activation was associated with both increased audiovisual and pain intrusion frequency.Conclusions: Enhanced AI and dACC processing during aversive films, poor pain vs. no-pain discrimination in AI and dACC, as well as weak regulatory VMPFC processing may be driving factors for intrusion formation, particularly in combination with high lifetime adversity. Results shed light on a potential path for the etiology of PTSD and medically unexplained pain.

AI and dACC play a common role for both trauma- and pain-processing.In combination with high lifetime adversity, higher AI and dACC aversive film processing was associated with higher audiovisual intrusion frequency, whereas weaker AI and dACC pain discrimination enhanced the chance for pain intrusions.Weak regulatory VMPFC activity in aversive situations increased both audiovisual and pain intrusion formation.

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The objective of this constructivist grounded theory study was to understand the experiences of students who have been disciplinarily excluded from school. Fifteen students (male, n = 11; Black, n = 10; having special education needs, n = 9) and 16 multidisciplinary staff in Ontario participated. Students experienced high rates of expanded adversities, including school and community violence, systemic racism and inequity. The importance of connection wove throughout the data; however, three themes were found to block connection: unacknowledged impact of adversity, a climate of fear, and the disproportionate impact of limited resources. Trauma-informed culturally attuned approaches that focus on the disproportionate impact of adversity and school discipline at the point of a disciplinary response, and throughout a student's educational experience, are essential.

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Caregiving adversity (CA) exposure is robustly linked to increased risk for poor oral, physical, and mental health outcomes. Increasingly, the gut microbiome has garnered interest as a contributor to risk for and resilience to such health outcomes in CA-exposed individuals. Though often overlooked, the oral microbiome of CA-exposed individuals may be just as important a contributor to health outcomes as the gut microbiome. Indeed, outside the context of CA, the oral microbiome is well-documented as a regulator of both oral and systemic health, and preliminary data suggest its association with mental health. However, research examining the association between CA and the oral microbiome is extremely sparse, especially in childhood, when the community composition of such organisms is still stabilizing. To address that sparsity, in the current study, we examined composition and differential abundance metrics of the oral microbiome in 152 youth aged 6-16 years, who had either been exposed to significant caregiving adversity (significant separation from or maltreatment by a caregiver; N = 66, CA) or who had always remained with their biological/birth families (N = 86, Comparison). We identified a significant negative association between hair cortisol and oral microbiome richness in the Comparison group that was significantly blunted in the CA group. Additionally, youth in the CA group had altered oral microbiome composition and elevated abundance of potentially pathogenic bacteria relative to youth in the Comparison group. Questionnaire measures of fatigue, somatic complaints, and internalizing symptoms had limited associations with oral microbiome features that were altered in CA. Although we found differences in the oral microbiomes of CA-exposed youth, further research is required to elucidate the implications of those differences for health and well-being.

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BACKGROUND: Adverse childhood experiences (ACEs) affect up to half the general population, they are known to co-occur, and are particularly common among those experiencing poverty. Yet, there are limited studies examining specific patterns of ACE co-occurrence considering their developmental timing. OBJECTIVE: To examine the longitudinal co-occurrence patterns of ACEs across childhood and adolescence, and to examine the role of poverty in predicting these. PARTICIPANTS AND SETTING: The sample was 8859 children from the Avon Longitudinal Study of Parents and Children, a longitudinal prospective population-based UK birth cohort. METHODS: Repeated measures of ten ACEs were available, occurring in early childhood (birth-5 years), mid-childhood (6-10 years), and adolescence (11-16 years). Latent class analysis was used to identify groups of children with similar developmental patterns of ACEs. Multinomial regression was used to examine the association between poverty during pregnancy and ACE classes. RESULTS: Sixteen percent of parents experienced poverty. A five-class latent model was selected: "Low ACEs" (72·0 %), "Early and mid-childhood household disharmony" (10·6 %), "Persistent parental mental health problems" (9·7 %), "Early childhood abuse and parental mental health problems" (5·0 %), and "Mid-childhood and adolescence ACEs" (2·6 %). Poverty was associated with a higher likelihood of being in each of the ACE classes compared to the low ACEs reference class. The largest effect size was seen for the "Early and mid-childhood household disharmony" class (OR 4·70, 95 % CI 3·68-6·00). CONCLUSIONS: A multifactorial approach to preventing ACEs is needed - including support for parents facing financial and material hardship, at-risk families, and timely interventions for those experiencing ACEs.

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BACKGROUND: Over 60 % of U.S. adults report adverse childhood experience (ACE), which correlate with risky health behaviors and lower utilization of healthcare preventive measures, potentially leading to chronic diseases in later life. OBJECTIVE: This study investigates the relationship between ACEs and human papillomavirus (HPV) vaccination in a national U.S. adult sample. PARTICIPANTS AND SETTING: We used data from selected states from the Centers for Disease Control and Prevention Behavioral Risk Factor Surveillance System collected in years 2019 (Mississippi, South Carolina, and Tennessee), 2020 (Georgia, Mississippi, North Dakota, South Carolina), 2021 (Mississippi), and 2022 (Arkansas) (N = 3578, 4392, 904, and 810, respectively). METHODS: We conducted descriptive, univariate, and multivariable regression analysis using SAS 9.4. Independent and dependent variables were ACEs and HPV vaccination, respectively. RESULTS: Individuals with ≥4 ACEs, versus no ACEs, were significantly more likely to report HPV vaccination in 2019, 2020, and 2021 (OR = 1.40, 1.77, 2.80, all p < 0.05 respectively), except in 2022 (OR = 1.54, p = 0.165). In 2019, specific ACE types, emotional abuse, and household mental illness were associated with HPV vaccination, whereas in 2021, emotional abuse, household mental illness, incarcerated household member, and substance abuse in household, and in 2022, emotional abuse was associated with HPV vaccination. CONCLUSIONS: We found mostly positive association between ACEs and HPV vaccination, particularly in initial three years. However, findings in 2022 were not significant, except for emotional abuse. Diverse patterns in relationship between ACEs and HPV vaccination was observed overtime, highlighting the need for consistency in ACEs and HPV vaccination data collection, including vaccination timing, to better understand the underlying mechanisms and plan for interventions to prevent HPV-related cancers among these populations.

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Background: Exposure to adversity, including unpredictable environments, during early life is associated with neuropsychiatric illness in adulthood. One common factor in this sequela is anhedonia, the loss of responsivity to previously reinforcing stimuli. To accelerate the development of new treatment strategies for anhedonic disorders induced by early-life adversity, animal models have been developed to capture critical features of early-life stress and the behavioral deficits that such stressors induce. We have previously shown that rats exposed to the limited bedding and nesting protocol exhibited blunted reward responsivity in the probabilistic reward task, a touchscreen-based task reverse translated from human studies. Methods: To test the quantitative limits of this translational platform, we examined the ability of Bayesian computational modeling and probability analyses identical to those optimized in previous human studies to quantify the putative mechanisms that underlie these deficits with precision. Specifically, 2 parameters that have been shown to independently contribute to probabilistic reward task outcomes in patient populations, reward sensitivity and learning rate, were extracted, as were trial-by-trial probability analyses of choices as a function of the preceding trial. Results: Significant deficits in reward sensitivity, but not learning rate, contributed to the anhedonic phenotypes in rats exposed to early-life adversity. Conclusions: The current findings confirm and extend the translational value of these rodent models by verifying the effectiveness of computational modeling in distinguishing independent features of reward sensitivity and learning rate that complement the probabilistic reward task's signal detection end points. Together, these metrics serve to objectively quantify reinforcement learning deficits associated with anhedonic phenotypes.

Exposure to early-life adversity can lead to psychiatric illness, including anhedonia, the loss of pleasure from previously rewarding activities. This article describes findings from rats exposed to a model of simulated poverty on a touchscreen-based assay reverse translated from a task used to characterize anhedonia in humans. We documented the ability of Bayesian computational modeling and probability analyses, identical to those used with humans, to objectively quantify reinforcement learning deficits associated with anhedonia in rats.

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Addressing the tremendous burden of early-life adversity requires constructive dialogues between scientists and policy makers to improve population health. Whereas dialogues focused on several aspects of early-life adversity have been initiated, discussion of an underrecognized form of adversity that has been observed across multiple contexts and cultures is only now emerging. Here we provide evidence for "why unpredictability?", including: 1. Evidence that exposures to unpredictability affect child neurodevelopment, with influences that persist into adulthood. 2. The existence of a translational non-human animal model of exposure to early life unpredictability that can be capitalized upon to causally probe neurobiological mechanisms. 3. Evidence that patterns of signals in the early environment promote brain maturation across species. 4. The uneven distribution of unpredictability across demographic populations that illuminates a possible focal point for enhancing health equity. We then outline the potential of unpredictability in terms of the "what"; that is, how might the concept of unpredictability be leveraged to inform policy? We emphasize the importance of interdisciplinary and community partnerships to the success of this work and describe our community-engaged research project. Finally, we highlight opportunities for the science of unpredictability to inform policies in areas such as screening, immigration, criminal justice, education, childcare, child welfare, employment, healthcare and housing.

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Individuals considered resilient can overcome adversity, achieving normal physical and psychological development, while those deemed vulnerable may not. Adversity promotes structural and functional alterations in the medial prefrontal cortex (mPFC) and hippocampus. Moreover, activity-dependent synaptic plasticity is intricately linked to neuronal shaping resulting from experiences. We hypothesize that this plasticity plays a crucial role in resilience processes. However, there is a notable absence of studies investigating this plasticity and behavioral changes following social adversity at different life stages. Consequently, we evaluated the impact of social adversity during early postnatal development (maternal separation [MS]), adulthood (social defeat [SD]), and a combined exposure (MS + SD) on behavioral outcomes (anxiety, motivation, anhedonia, and social interaction). We also examined cFos expression induced by social interaction in mPFC and hippocampus of adult male rats. Behavioral analyses revealed that SD-induced anhedonia, whereas MS + SD increased social interaction and mitigated SD-induced anhedonia. cFos evaluation showed that social interaction heightened plasticity in the prelimbic (PrL) and infralimbic (IL) cortices, dentate gyrus (DG), CA3, and CA1. Social interaction-associated plasticity was compromised in IL and PrL cortices of the MS and SD groups. Interestingly, social interaction-induced plasticity was restored in the MS + SD group. Furthermore, plasticity was impaired in DG by all social stressors, and in CA3 was impaired by SD. Our findings suggest in male rats (i) two adverse social experiences during development foster resilience; (ii) activity-dependent plasticity in the mPFC is a foundation for resilience to social adversity; (iii) plasticity in DG is highly susceptible to social adversity.

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Treatment with antipsychotics (APs) for schizophrenia spectrum disorders (SSDs) is generally effective, however, a significant proportion does not respond favorably. Childhood trauma (CT) subtypes (physical, sexual, and emotional abuse, physical and emotional neglect) could influence treatment effectiveness; however, research is scarce. Heterogeneity in AP response could be explained by differentiating by CT subtype. The present study was based on the Bergen-Stavanger-Trondheim-Innsbruck (BeSt InTro) study. CTQ-SF assessed CT subtypes in SSDs (n = 98). CT subtypes were examined in relation to psychosis symptoms measured by PANSS during one year of treatment with APs, by means of linear mixed effects (LME) models. Results were significant for CT subtypes, where increased levels of sexual abuse and physical neglect were associated with increased mean levels of psychosis symptoms throughout the course of treatment from baseline to 52 weeks. AP effectiveness may thus be influenced by CT subtype in SSDs. The results support clinical guidelines recommending a focus on assessment and treatment of trauma in SSDs.

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BACKGROUND: Childhood adversity has been associated with alterations in threat-related information processing, including heightened perceptual sensitivity and attention bias towards threatening facial expressions, as well as hostile attributions of neutral faces, although there is a large degree of variability and inconsistency in reported findings. METHODS: Here, we aimed to implicitly measure neural facial expression processing in 120 adolescents between 12 and 16 years old with and without exposure to childhood adversity. Participants were excluded if they had any major medical or neurological disorder or intellectual disability, were pregnant, used psychotropic medication or reported acute suicidality or an ongoing abusive situation. We combined fast periodic visual stimulation with electroencephalography in two separate paradigms to assess the neural sensitivity and responsivity towards neutral and expressive, i.e. happy and angry, faces. Linear mixed effects models were used to assess the impact of childhood adversity on facial expression processing. RESULTS: Sixty-six girls, 53 boys and one adolescent who identified as 'other', between 12 and 16 years old (M = 13.93), participated in the current study. Of those, 64 participants were exposed to childhood adversity. In contrast to our hypotheses, adolescents exposed to adversity show lower expression-discrimination responses for angry faces presented in between neutral faces and higher expression-discrimination responses for happy faces presented in between neutral faces than unexposed controls. Moreover, adolescents exposed to adversity, but not unexposed controls, showed lower neural responsivity to both angry and neutral faces that were simultaneously presented. CONCLUSIONS: We therefore conclude that childhood adversity is associated with a hostile attribution of neutral faces, thereby reducing the dissimilarity between neutral and angry faces. This reduced threat-safety discrimination may increase risk for psychopathology in individuals exposed to childhood adversity.

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Background: Resilience refers to the process of demonstrating better outcomes than would be expected based on the adversity one experienced. Resilience is increasingly measured using a residual approach, which typically assesses adversity and mental health outcomes over a longitudinal timeframe. It remains unknown to what extent such a residual-based measurement of resilience is sensitive to variation in acute stress resilience, a candidate resilience factor. Methods: Fifty-seven emerging adults enrolled in tertiary education completed measures of adversity and emotional experiences. To assess stress recovery, participants were exposed to a lab-based adverse event from which a Laboratory Stress Resilience Index was derived. Results: We derived a residual-based measure of emotional resilience from regressing emotional experience scores onto adversity scores. This residual-based measure of emotional resilience predicted variance in the Laboratory Stress Resilience Index over and above that predicted by both a traditional resilience measure and the emotional experiences measure. These findings suggest that acute stress resilience may be a factor underpinning variation in emotional resilience, and that the residual-based approach to measuring resilience is sensitive to such variation in stress resilience.

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BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

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The adversity faced by left-behind children due to parental migration affects their depressive symptoms, but little is known about the mechanism underlying this association and protective factors from a dynamic perspective. The present study examined the association between family adversity and the developmental trajectory of depressive symptoms, and the potential mediating and moderating role of personal growth initiative in this association among left-behind children. A total of 363 left-behind children (48.8% female; Mage = 12.97 at T1, SDage = 0.55) from five rural middle schools in the Hunan Province of China participated in this three-wave study, employing one-year intervals between assessments. The results indicated the initial level of personal growth initiative mediated the association between family adversity at T1 and the development of depressive symptoms, while the growth rate of personal growth initiative both mediated and moderated this association, with consistent effects across sexes. These findings underscore the critical role of personal growth initiative in the association between family adversity and depressive symptoms among left-behind children.

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OBJECTIVES: The objective of this study was to develop Service, Research and Policy priorities to prevent the impact of family adversity on child mental health and determine comparative priorities of diverse stakeholders to those with lived experience of adversity. METHODS: Value-weighting approach conducted in a staged process: (i) professionals and experts with lived experience from health, education, justice and social care sectors attended a national symposium to identify priorities for family adversity and mental health and (ii) a subsequent resource allocation survey gathered views from participants and external experts on symposium priorities. RESULTS: Consensus was reached on priorities. Service priorities included establishing intersectoral hubs for children and families and early childhood nurse home-visiting programs. Research priorities included scaling up evidence-based interventions and evaluating cross-sector, flexible funding models for services addressing childhood adversity. Policy priorities included developing evidence-based policies with evaluation and implementation plans and flexible funding models to support integrated care. CONCLUSIONS: Our results provide detailed and actionable clarity on next steps to address family adversities. IMPLICATIONS FOR PUBLIC HEALTH: The priorities call for a focus on cross-sectoral approaches to preventing or mitigating the effects of family adversity. The current Australian policy environment provides a timely opportunity to action the proposed interventions.

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Inflammation likely mediates associations between nicotine use and negative health outcomes. Sex differences have been observed in nicotine use-inflammation links, and physiological processes during puberty might allow for these differences to arise. In this cross-sectional study of 498 youth (ages 8-13, 52% girls, 77% with history of child maltreatment (CM) investigation), sex-differentiated associations between self-reported nicotine use and high-sensitivity C-reactive protein (hs-CRP) were explored. Additionally, self-reported pubertal stage was investigated as a moderator of such nicotine use-hs-CRP links. Hierarchical generalized estimating equation models were adjusted for a wide range of adversity effects: CM investigation history derived from state records, self- and caregiver-report of traumatic life events, adversity-related demographic risk factors (i.e., identification with historically marginalized racial and ethnic groups, household income), and other characteristics that may influence the variables of interest (e.g., medication use, age, body mass index). Nicotine use had a negative main effect on hs-CRP among boys (ß = -0.50, p = 0.02), and pubertal stage did not moderate this association (ß = 0.06, p = 0.71). In contrast, pubertal stage moderated the association between nicotine use and hs-CRP among girls (ß = 0.48, p = 0.02) such that a positive association between nicotine use and hs-CRP levels was stronger at more advanced pubertal stages (ß = 0.45, SE = 0.21, 95% CI [0.03, 0.87]). Findings suggest that puberty may influence the effect of nicotine on inflammation in sex-differentiated ways and have implications for timing of prevention and treatment efforts geared toward reducing nicotine use and subsequent inflammation-related health risk among youth.

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BACKGROUND AND AIMS: Early-life adversities are known to alter drug reward processing in rodents. Despite the well-known link between early adversity and the risk of substance use disorder, few studies have measured how childhood adversity affects human drug reward. Here, we assessed the relationship between historical childhood adversities and responses to single doses of methamphetamine, d-amphetamine or buprenorphine in healthy participants. METHODS: Using a secondary analysis approach, we assessed the impact of childhood adversity on drug effects from three randomised, placebo-controlled studies in which healthy volunteers received methamphetamine (20 mg oral; n = 35), d-amphetamine (20 mg oral; n = 54) or buprenorphine (0.2 mg sublingual; n = 35). Ratings of feeling effect, liking, disliking, feeling high and wanting more of the drug were collected 15-210 min post-administration, and heart rate changes were analysed using random-intercept mixed-effect models. The area under the curve from these and previous studies was calculated to visualise the relationship between childhood adversity severity and drug effects. RESULTS: Greater childhood adversity was associated with reduced feel effects (significant three-way interactions b = -0.07, 95% CI [-0.12, -0.02], p = 0.009), like effects (b = -0.07, 95% CI [-0.13, -0.00], p = 0.038) and feel high (b = -0.06, 95% CI [-0.10, -0.01], p = 0.020) towards the stimulant drugs 90-180 min post-administration. CONCLUSIONS: Childhood adversity was not significantly associated with other subjective or heart rate responses to the drugs. Overall, participants with more childhood adversities reported dampened subjective responses to stimulant drugs, but not to buprenorphine. Future studies should examine the generalisability of these relationships, to identify the mechanisms underlying the link between childhood adversity and drug responsiveness.

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BACKGROUND: Violence exposure during childhood and adolescence is associated with increased prevalence and severity of psychopathology. Neurobiological correlates suggest that abnormal maturation of emotion-related brain circuitry, such as amygdala-prefrontal cortex (PFC), may underlie the development of psychiatric symptoms after exposure; however, it remains unclear how amygdala-PFC circuit maturation is related to psychiatric risk in the context of violence. METHODS: This study analyzed individual differences in amygdala-PFC circuit maturity using data collected from the Philadelphia Neurodevelopmental Cohort (PNC; N=1,133 youth). Neurodevelopment models of amygdala-PFC resting-state functional connectivity were built using deep learning, trained to predict chronological age in typically developing youth (neither violence exposed nor having a psychiatric diagnosis). Using the brain age gap estimate (BrainAGE), an index of relative circuit maturation, patterns of atypical neurodevelopment were interrogated. RESULTS: Violence exposure was associated with delayed maturation of basolateral amygdala (BLA) - PFC circuits, driven by increased BLA - medial orbitofrontal cortex functional connectivity. Increased psychiatric symptoms, on the other hand, was associated with advanced maturation of BLA - PFC functional connectivity, driven by decreased BLA - dorsolateral PFC functional connectivity. CONCLUSIONS: Delayed frontoamygdala maturation after exposure to violence suggests atypical, yet adaptive, development of threat appraisal processes, potentially reflecting greater threat generalization characteristic of younger children. Advanced circuit maturation with increasing symptoms suggests divergent neurodevelopmental mechanisms underlying illness after emotion-circuits have adapted to adversity, exacerbated by pre-existing vulnerabilities to early maturation. Disentangling the effects of adversity and psychopathology on neurodevelopment is crucial for helping youth recover from violence and preventing illness from continuing into adulthood.

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BACKGROUND: Children and young people (CYP) in contact with child welfare services are at high risk of developing mental health problems. There is a paucity of evidenced-based preventative interventions provided to this population. OBJECTIVE: This project worked in partnership with CYP, their parents/caregivers and the professionals who support them to co-produce a preventative mental health intervention for CYP in contact with child welfare services. PARTICIPANTS AND SETTING: We recruited a purposive sample of CYP in contact with child welfare services (n = 23), parents/caregivers (n = 18) and practitioners working within child welfare services and mental health services (n = 25) from the North East of England and convened co-production workshops (n = 4). METHODS: This project followed the established principles for intervention development, applying the six steps to quality intervention development (6SQUID) approach. The mixed method research consisted of four work packages with continuous engagement of stakeholders throughout the project. These were: a systematic review of reviews; focus groups with practitioners; interviews with parents/caregivers and CYP; co-production workshops. RESULTS: We identified that the primary risk factor affecting CYP in contact with child welfare services is the experience of childhood adversity. The quality of relationships that the CYP experiences with both their parent/caregivers and the professionals involved in their care are considered to be the main factors amenable to change. CONCLUSIONS: We found that a trauma-informed, activity-based intervention with an embedded family-focused component provided to CYP who have experienced adversity is most likely to prevent mental health problems in those in contact with child welfare services.

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