Robust genetic nurture effects on education: A systematic review and meta-analysis based on 38,654 families across 8 cohorts.

Similarities between parents and offspring arise from nature and nurture. Beyond this simple dichotomy, recent genomic studies have uncovered "genetic nurture" effects, whereby parental genotypes influence offspring outcomes via environmental pathways rather than genetic transmission. Such genetic nurture effects also need to be accounted for to accurately estimate "direct" genetic effects (i.e., genetic effects on a trait originating in the offspring). Empirical studies have indicated that genetic nurture effects are particularly relevant to the intergenerational transmission of risk for child educational outcomes, which are, in turn, associated with major psychological and health milestones throughout the life course. These findings have yet to be systematically appraised across contexts. We conducted a systematic review and meta-analysis to quantify genetic nurture effects on educational outcomes. A total of 12 studies comprising 38,654 distinct parent(s)-offspring pairs or trios from 8 cohorts reported 22 estimates of genetic nurture effects. Genetic nurture effects on offspring's educational outcomes (ßgenetic nurture = 0.08, 95% CI [0.07, 0.09]) were smaller than direct genetic effects (ßdirect genetic = 0.17, 95% CI [0.13, 0.20]). Findings were largely consistent across studies. Genetic nurture effects originating from mothers and fathers were of similar magnitude, highlighting the need for a greater inclusion of fathers in educational research. Genetic nurture effects were largely explained by observed parental education and socioeconomic status, pointing to their role in environmental pathways shaping child educational outcomes. Findings provide consistent evidence that environmentally mediated parental genetic influences contribute to the intergenerational transmission of educational outcomes, in addition to effects due to genetic transmission.

Editorial Perspective: Misaligned incentives in mental health research - the case for Registered Reports.

Current incentive structures reward mental health researchers for producing positive, novel, and clean results. This can promote questionable research practices which contribute to a distorted evidence base, in turn limiting progress in mental health research. Registered Reports (RRs) offer a solution to realign the incentives towards conducting high-quality, rigorous, and accurate studies, by preventing publication and reporting biases. However, the uptake of RRs in mental health research has so far been limited. This editorial perspective highlights the advantages of RRs for mental health research, before discussing potential challenges and how they can be addressed. Greater uptake of RRs in mental health research could help to promote a fairer research culture, limit publication bias and questionable research practices, and ultimately, improve understanding of mental health.

The relationship between type, timing and duration of exposure to adverse childhood experiences and adolescent self-harm and depression: findings from three UK prospective population-based cohorts.

BACKGROUND: Adverse childhood experiences (ACEs) are well-established risk factors for self-harm and depression. However, despite their high comorbidity, there has been little focus on the impact of developmental timing and the duration of exposure to ACEs on co-occurring self-harm and depression. METHODS: Data were utilised from over 22,000 children and adolescents participating in three UK cohorts, followed up longitudinally for 14-18 years: the Avon Longitudinal Study of Parents and Children (ALSPAC), the Millennium Cohort Study (MCS) and the Environmental Risk (E-Risk) Longitudinal Twin Study. Multinomial logistic regression models estimated associations between each ACE type and a four-category outcome: no self-harm or depression, self-harm alone, depression alone and self-harm with co-occurring depression. A structured life course modelling approach was used to examine whether the accumulation (duration) of exposure to each ACE, or a critical period (timing of ACEs) had the strongest effects on self-harm and depression in adolescence. RESULTS: The majority of ACEs were associated with co-occurring self-harm and depression, with consistent findings across cohorts. The importance of timing and duration of ACEs differed across ACEs and across cohorts. For parental mental health problems, longer duration of exposure was strongly associated with co-occurring self-harm and depression in both ALSPAC (adjusted OR: 1.18, 95% CI: 1.10-1.25) and MCS (1.18, 1.11-1.26) cohorts. For other ACEs in ALSPAC, exposure in middle childhood was most strongly associated with co-occurring self-harm and depression, and ACE occurrence in early childhood and adolescence was more important in the MCS. CONCLUSIONS: Efforts to mitigate the impact of ACEs should start in early life with continued support throughout childhood, to prevent long-term exposure to ACEs contributing to risk of self-harm and depression in adolescence.

Subjective and objective experiences of childhood adversity: a meta-analysis of their agreement and relationships with psychopathology.

BACKGROUND: Researchers use both subjective self-report and objective measures, such as official records, to investigate the impact of childhood adversity on psychopathology. However, it is unclear whether subjective and objective measures of childhood adversity (a) show agreement, and (b) differentially predict psychopathology. METHOD: To address this, we conducted a pre-registered meta-analysis to examine the agreement between subjective and objective measures of childhood adversity, and their prediction of psychopathology. We searched in PubMed, PsycINFO and Embase for articles with both subjective measures (self-reports) and objective measures of childhood adversity (comprising official records, or reports from multiple informants unrelated to the target individual), and measures of psychopathology. RESULTS: We identified 22 studies (n = 18,163) with data on agreement between subjective and objective measures of childhood adversities, and 17 studies (n = 14,789) with data on the associations between subjective and objective measures with psychopathology. First, we found that subjective and objective measures of childhood adversities were only moderately correlated (e.g. for maltreatment, r = .32, 95% CI = 0.23-0.41). Second, subjective measures of childhood adversities were associated with psychopathology, independent of objective measures (e.g. for maltreatment, r = .16, 95% CI = 0.09-0.22). In contrast, objective measures of childhood adversities had null or minimal associations with psychopathology, independent of subjective measures (e.g. r for maltreatment = .06, 95% CI = -0.02-0.13). CONCLUSIONS: Our findings suggest that the effects of childhood adversity on psychopathology are primarily driven by a person's subjective experience. If this is the case, clinical interventions targeting memories and cognitive processes surrounding childhood adversity may reduce the risk of psychopathology in exposed individuals.

Early risk factors for joint trajectories of bullying victimisation and perpetration.

Bullying victimisation is a prevalent stressor associated with serious health problems. To inform intervention strategies, it is important to understand children's patterns of involvement in bullying victimisation and perpetration across development, and identify early risk factors for these developmental trajectories. We analysed data from the Millennium Cohort Study (N = 14,525; 48.6% female, 82.6% White), a representative birth cohort of British children born in 2000-2002 across the UK. Bullying victimisation and perpetration were assessed via child, mother, and teacher reports at ages 5, 7, 11, and 14 years. Early risk factors (child emotional, cognitive, and physical vulnerabilities, and adverse family environments) were assessed at ages 9 months, 3, and 5 years. Using k-means for longitudinal data, we identified five joint trajectories of victimisation and perpetration across ages 5, 7, 11, and 14: uninvolved children (59.78%), early child victims (9.96%), early adolescent victims (15.07%), early child bullies (8.01%), and bully- victims (7.19%). Individual vulnerabilities (e.g., emotional dysregulation, cognitive difficulties) and adverse family environments (maternal psychopathology, low income) in pre-school years independently forecast multiple trajectories of bullying involvement. Compared to victims, bully-victims were more likely to be male, have cognitive difficulties, and experience harsh discipline and low income. Interventions addressing these risk factors (e.g., via accessible mental health care, stigma-based interventions, or programs to support low-income families) may help to prevent bullying involvement and its associated sequelae.

Genetic and early environmental predictors of adulthood self-reports of trauma.

BACKGROUND: Retrospective self-reports of childhood trauma are associated with a greater risk of psychopathology in adulthood than prospective measures of trauma. Heritable reporter characteristics are anticipated to account for part of this association, whereby genetic predisposition to certain traits influences both the likelihood of self-reporting trauma and of developing psychopathology. However, previous research has not considered how gene-environment correlation influences these associations. AIMS: To investigate reporter characteristics associated with retrospective self-reports of childhood trauma and whether these associations are accounted for by gene-environment correlation. METHOD: In 3963 unrelated individuals from the Twins Early Development Study, we tested whether polygenic scores for 21 psychiatric, cognitive, anthropometric and personality traits were associated with retrospectively self-reported childhood emotional and physical abuse. To assess the presence of gene-environment correlation, we investigated whether these associations remained after controlling for composite scores of environmental adversity across development. RESULTS: Retrospectively self-reported childhood trauma was associated with polygenic scores for autism spectrum disorder (ASD), body mass index (BMI), post-traumatic stress disorder (PTSD) and risky behaviours. When composite scores of environmental adversity were controlled for, only associations with the polygenic scores for ASD and PTSD remained significant. CONCLUSIONS: Genetic predisposition to ASD and PTSD may increase liability to experiencing or interpreting events as traumatic. Associations between genetic predisposition for risky behaviour and BMI with self-reported childhood trauma may reflect gene-environment correlation. Studies of the association between retrospectively self-reported childhood trauma and later-life outcomes should consider that genetically influenced reporter characteristics may confound associations, both directly and through gene-environment correlation.

Research Review: A guide to computing and implementing polygenic scores in developmental research.

The increasing availability of genotype data in longitudinal population- and family-based samples provides opportunities for using polygenic scores (PGS) to study developmental questions in child and adolescent psychology and psychiatry. Here, we aim to provide a comprehensive overview of how PGS can be generated and implemented in developmental psycho(patho)logy, with a focus on longitudinal designs. As such, the paper is organized into three parts: First, we provide a formal definition of polygenic scores and related concepts, focusing on assumptions and limitations. Second, we give a general overview of the methods used to compute polygenic scores, ranging from the classic approach to more advanced methods. We include recommendations and reference resources available to researchers aiming to conduct PGS analyses. Finally, we focus on the practical applications of PGS in the analysis of longitudinal data. We describe how PGS have been used to research developmental outcomes, and how they can be applied to longitudinal data to address developmental questions.

Research Review: How to interpret associations between polygenic scores, environmental risks, and phenotypes.

BACKGROUND: Genetic influences are ubiquitous as virtually all phenotypes and most exposures typically classified as environmental have been found to be heritable. A polygenic score summarises the associations between millions of genetic variants and an outcome in a single value for each individual. Ever lowering costs have enabled the genotyping of many samples relevant to child psychology and psychiatry research, including cohort studies, leading to the proliferation of polygenic score studies. It is tempting to assume that associations detected between polygenic scores and phenotypes in those studies only reflect genetic effects. However, such associations can reflect many pathways (e.g. via environmental mediation) and biases. METHODS: Here, we provide a comprehensive overview of the many reasons why associations between polygenic scores, environmental exposures, and phenotypes exist. We include formal representations of common analyses in polygenic score studies using structural equation modelling. We derive biases, provide illustrative empirical examples and, when possible, mention steps that can be taken to alleviate those biases. RESULTS: Structural equation models and derivations show the many complexities arising from jointly modelling polygenic scores with environmental exposures and phenotypes. Counter-intuitive examples include that: (a) associations between polygenic scores and phenotypes may exist even in the absence of direct genetic effects; (b) associations between child polygenic scores and environmental exposures can exist in the absence of evocative/active gene-environment correlations; and (c) adjusting an exposure-outcome association for a polygenic score can increase rather than decrease bias. CONCLUSIONS: Strikingly, using polygenic scores may, in some cases, lead to more bias than not using them. Appropriately conducting and interpreting polygenic score studies thus requires researchers in child psychology and psychiatry and beyond to be versed in both epidemiological and genetic methods or build on interdisciplinary collaborations.

Protecting against researcher bias in secondary data analysis: challenges and potential solutions.

Analysis of secondary data sources (such as cohort studies, survey data, and administrative records) has the potential to provide answers to science and society's most pressing questions. However, researcher biases can lead to questionable research practices in secondary data analysis, which can distort the evidence base. While pre-registration can help to protect against researcher biases, it presents challenges for secondary data analysis. In this article, we describe these challenges and propose novel solutions and alternative approaches. Proposed solutions include approaches to (1) address bias linked to prior knowledge of the data, (2) enable pre-registration of non-hypothesis-driven research, (3) help ensure that pre-registered analyses will be appropriate for the data, and (4) address difficulties arising from reduced analytic flexibility in pre-registration. For each solution, we provide guidance on implementation for researchers and data guardians. The adoption of these practices can help to protect against researcher bias in secondary data analysis, to improve the robustness of research based on existing data.

Cyber-victimisation and mental health in young people: a co-twin control study.

BACKGROUND: The rise of social media use in young people has sparked concern about the impact of cyber-victimisation on mental health. Although cyber-victimisation is associated with mental health problems, it is not known whether such associations reflect genetic and environmental confounding. METHODS: We used the co-twin control design to test the direct association between cyber-victimisation and multiple domains of mental health in young people. Participants were 7708 twins drawn from the Twins Early Development Study, a UK-based population cohort followed from birth to age 22. RESULTS: Monozygotic twins exposed to greater levels of cyber-victimisation had more symptoms of internalising, externalising and psychotic disorders than their less victimised co-twins at age 22, even after accounting for face-to-face peer victimisation and prior mental health. However, effect sizes from the most stringent monozygotic co-twin control analyses were decreased by two thirds from associations at the individual level [pooled ß across all mental health problems = 0.06 (95% CI 0.03-0.10) v. 0.17 (95% CI 0.15-0.19) in individual-level analyses]. CONCLUSIONS: Cyber-victimisation has a small direct association with multiple mental health problems in young people. However, a large part of the association between cyber-victimisation and mental health is due to pre-existing genetic and environmental vulnerabilities and co-occurring face-to-face victimisation. Therefore, preventative interventions should target cyber-victimisation in conjunction with pre-existing mental health vulnerabilities and other forms of victimisation.

Childhood victimization and inflammation in young adulthood: A genetically sensitive cohort study.

OBJECTIVE: Childhood victimization is an important risk factor for later immune-related disorders. Previous evidence has demonstrated that childhood victimization is associated with elevated levels of inflammation biomarkers measured decades after exposure. However, it is unclear whether this association is (1) already detectable in young people, (2) different in males and females, and (3) confounded by genetic liability to inflammation. Here we sought to address these questions. METHOD: Participants were 2232 children followed from birth to age 18years as part of the Environmental Risk (E-Risk) Longitudinal Twin Study. Childhood victimization was measured prospectively from birth to age 12years. Inflammation was measured through C-reactive protein (CRP) levels in dried blood spots at age 18years. Latent genetic liability for high inflammation levels was assessed through a twin-based method. RESULTS: Greater exposure to childhood victimization was associated with higher CRP levels at age 18 (serum-equivalent means were 0.65 in non-victimized Study members, 0.74 in those exposed to one victimization type, and 0.81 in those exposed to poly-victimization; p=0.018). However, this association was driven by a significant association in females (serum-equivalent means were 0.75 in non-victimized females, 0.87 in those exposed to one type of victimization, and 1.19 in those exposed to poly-victimization; p=0.010), while no significant association was observed in males (p=0.19). Victimized females showed elevated CRP levels independent of latent genetic influence, as well as childhood socioeconomic status, and waist-hip ratio and body temperature at the time of CRP assessment. CONCLUSION: Childhood victimization is associated with elevated CRP levels in young women, independent of latent genetic influences and other key risk factors. These results strengthen causal inference about the effects of childhood victimization on inflammation levels in females by accounting for potential genetic confounding.

Hidden Wounds? Inflammatory Links Between Childhood Trauma and Psychopathology.

Childhood trauma is a key risk factor for psychopathology. However, little is known about how exposure to childhood trauma is translated into biological risk for psychopathology. Observational human studies and experimental animal models suggest that childhood exposure to stress can trigger an enduring systemic inflammatory response not unlike the bodily response to physical injury. In turn, these "hidden wounds" of childhood trauma can affect brain development, key behavioral domains (e.g., cognition, positive valence systems, negative valence systems), reactivity to subsequent stressors, and, ultimately, risk for psychopathology. Further research is needed to better characterize the inflammatory links between childhood trauma and psychopathology. Detecting and healing these hidden wounds may help prevent and treat psychopathology emerging after childhood trauma.

In the eye of the beholder: Perceptions of neighborhood adversity and psychotic experiences in adolescence.

Adolescent psychotic experiences increase risk for schizophrenia and other severe psychopathology in adulthood. Converging evidence implicates urban and adverse neighborhood conditions in the etiology of adolescent psychotic experiences, but the role of young people's personal perceptions of disorder (i.e., physical and social signs of threat) in their neighborhood is unknown. This was examined using data from the Environmental Risk Longitudinal Twin Study, a nationally representative birth cohort of 2,232 British twins. Participants were interviewed at age 18 about psychotic phenomena and perceptions of disorder in the neighborhood. Multilevel, longitudinal, and genetically sensitive analyses investigated the association between perceptions of neighborhood disorder and adolescent psychotic experiences. Adolescents who perceived higher levels of neighborhood disorder were significantly more likely to have psychotic experiences, even after accounting for objectively/independently measured levels of crime and disorder, neighborhood- and family-level socioeconomic status, family psychiatric history, adolescent substance and mood problems, and childhood psychotic symptoms: odds ratio = 1.62, 95% confidence interval [1.27, 2.05], p < .001. The phenotypic overlap between adolescent psychotic experiences and perceptions of neighborhood disorder was explained by overlapping common environmental influences, rC = .88, 95% confidence interval [0.26, 1.00]. Findings suggest that early psychological interventions to prevent adolescent psychotic experiences should explore the role of young people's (potentially modifiable) perceptions of threatening neighborhood conditions.

Childhood Bullying Victimization and Overweight in Young Adulthood: A Cohort Study.

OBJECTIVE: To test whether bullied children have an elevated risk of being overweight in young adulthood and whether this association is: (1) consistent with a dose-response relationship, namely, its strength increases with the chronicity of victimization; (2) consistent across different measures of overweight; (3) specific to bullying and not explained by co-occurring maltreatment; (4) independent of key potential confounders; and (5) consistent with the temporal sequence of bullying preceding overweight. METHOD: A representative birth cohort of 2,232 children was followed to age 18 years as part of the Environmental Risk Longitudinal Twin Study. Childhood bullying victimization was reported by mothers and children during primary school and early secondary school. At the age-18 follow-up, we assessed a categorical measure of overweight, body mass index, and waist-hip ratio. Indicators of overweight were also collected at ages 10 and 12. Co-twin body mass and birth weight were used to index genetic and fetal liability to overweight, respectively. RESULTS: Bullied children were more likely to be overweight than non-bullied children at age 18, and this association was (1) strongest in chronically bullied children (odds ratio = 1.69; 95% confidence interval [CI] = 1.21-2.35); (2) consistent across measures of overweight (body mass index: b = 1.12; 95% CI = 0.37-1.87; waist-hip ratio: b = 1.76; 95% CI = 0.84-2.69); (3) specific to bullying and not explained by co-occurring maltreatment; (4) independent of child socioeconomic status, food insecurity, mental health, and cognition, and pubertal development; and (5) not present at the time of bullying victimization, and independent of childhood weight and genetic and fetal liability. CONCLUSION: Childhood bullying victimization predicts overweight in young adulthood.

Prospective and Retrospective Measures of Child Maltreatment and Their Association With Psychopathology: A Systematic Review and Meta-Analysis.

Importance: Prospective and retrospective measures of childhood maltreatment identify largely different groups of individuals. However, it is unclear if these measures are differentially associated with psychopathology. Objective: To analyze the associations of prospective and retrospective measures of childhood maltreatment with psychopathology. Data Sources: Based on a preregistered protocol, Embase, PsycInfo, and MEDLINE were searched for peer-reviewed studies published by January 1, 2023, that measured the associations of prospective and retrospective measures of child maltreatment with psychopathology. Study Selection: Titles and abstracts of all articles captured by the search and full texts of potentially eligible studies were independently screened by 2 authors. Observational studies with measures of the association of prospective and retrospective measures of childhood maltreatment with psychopathology were included. Data Extraction and Synthesis: Multiple investigators independently extracted data. Multilevel random-effects meta-analyses were used to pool the results and test predictors of heterogeneity. Main Outcome and Measures: Associations between prospective or retrospective measures of child maltreatment and psychopathology, both unadjusted and adjusted (ie, the association between prospective measures of maltreatment and psychopathology adjusted for retrospective measures, and vice versa), and moderation of these associations by preselected variables. Results: The meta-analyses were based on 24 studies including 15 485 individuals (51.0% female; mean age, 21.3 years at retrospective report). Retrospective measures of childhood maltreatment showed stronger associations with psychopathology relative to prospective measures in both unadjusted analyses (retrospective measures: odds ratio [OR], 2.21; 95%, 1.94-2.42 vs prospective measures: OR, 1.56; 95% CI, 1.39-1.76) and adjusted analyses (retrospective measures: OR, 2.14; 95% CI, 1.90-2.42 vs prospective measures: OR, 1.27; 95% CI, 1.13-1.41). There was no statistically significant moderation of the unadjusted or adjusted associations between prospective measures of child maltreatment and psychopathology. The associations between retrospective measures and psychopathology were stronger when the assessment of psychopathology was based on self-reports and was focused on internalizing or emotional disorders. Conclusions and Relevance: Psychopathology is more strongly associated with retrospective measures-which capture the first-person, subjective appraisal of childhood events reflected in memory recall-compared to prospective measures-which essentially capture third-person accounts of such events. Maltreatment-related psychopathology may be driven by subjective interpretations of experiences, distressing memories, and associated schemas, which could be targeted by cognitive interventions.

Assessing rates and predictors of cannabis-associated psychotic symptoms across observational, experimental and medical research.

Cannabis, one of the most widely used psychoactive substances worldwide, can give rise to acute cannabis-associated psychotic symptoms (CAPS). While distinct study designs have been used to examine CAPS, an overarching synthesis of the existing findings has not yet been carried forward. To that end, we quantitatively pooled the evidence on rates and predictors of CAPS (k = 162 studies, n = 210,283 cannabis-exposed individuals) as studied in (1) observational research, (2) experimental tetrahydrocannabinol (THC) studies, and (3) medicinal cannabis research. We found that rates of CAPS varied substantially across the study designs, given the high rates reported by observational and experimental research (19% and 21%, respectively) but not medicinal cannabis studies (2%). CAPS was predicted by THC administration (for example, single dose, Cohen's d = 0.7), mental health liabilities (for example, bipolar disorder, d = 0.8), dopamine activity (d = 0.4), younger age (d = -0.2), and female gender (d = -0.09). Neither candidate genes (for example, COMT, AKT1) nor other demographic variables (for example, education) predicted CAPS in meta-analytical models. The results reinforce the need to more closely monitor adverse cannabis-related outcomes in vulnerable individuals as these individuals may benefit most from harm-reduction efforts.

Burden of Mental Disorders and Suicide Attributable to Childhood Maltreatment.

Importance: The proportion of mental disorders and burden causally attributable to childhood maltreatment is unknown. Objective: To determine the contribution of child maltreatment to mental health conditions in Australia, accounting for genetic and environmental confounding. Design, Setting, and Participants: This meta-analysis involved an epidemiological assessment accounting for genetic and environmental confounding between maltreatment and mental health and 3 cross-sectional national surveys: the Australian Child Maltreatment Study (ACMS) 2023, National Study of Mental Health and Well-being 2020-2022, and Australian Burden of Disease Study 2023. Causal estimates were derived on the association between childhood maltreatment and mental health conditions from a meta-analysis of quasi-experimental studies. This was combined with the prevalence of maltreatment from the ACMS to calculate the population attributable fraction (PAF). The PAF was applied to the number and burden of mental health conditions in Australia, sourced from 2 population-based, nationally representative surveys of Australians aged 16 to 85 years, to generate the number and associated burden of mental disorders attributable to child maltreatment. Exposure: Physical abuse, sexual abuse, emotional abuse, or neglect prior to age 18 years. Main Outcomes and Measures: Proportion and number of cases, years of life lost, years lived with disability, and disability-adjusted life-years of mental health conditions (anxiety, depression, harmful alcohol and drug use, self-harm, and suicide attempt) attributable to childhood maltreatment. Results: Meta-analytic estimates were generated from 34 studies and 54 646 participants and applied to prevalence estimates of childhood maltreatment generated from 8503 Australians. Childhood maltreatment accounted for a substantial proportion of mental health conditions, ranging from 21% (95% CI, 13%-28%) for depression to 41% (95% CI, 27%-54%) of suicide attempts. More than 1.8 million cases of depressive, anxiety, and substance use disorders could be prevented if childhood maltreatment was eradicated. Maltreatment accounted for 66 143 years of life lost (95% CI, 43 313-87 314), primarily through suicide, and 184 636 disability-adjusted life-years (95% CI, 109 321-252 887). Conclusions and Relevance: This study provides the first estimates of the causal contribution of child maltreatment to mental health in Australia. Results highlight the urgency of preventing child maltreatment to reduce the population prevalence and burden of mental disorders.

Improving the Way that We Conceptualise Adverse Childhood Experiences - A Commentary on Sisitsky et al. (2023).

Research on adverse childhood experiences (ACEs) has traditionally relied on cumulative ACE scores, which prevents understanding about the effects of distinct adversities and their mechanistic pathways. Dimensional and person-centred approaches have been proposed as alternative methods to conceptualise ACEs, which address limitations of the cumulative ACE score. In this issue, Sisitsky et al. (Research on Child and Adolescent Psychopathology, 2023) apply these approaches to identify dimensions of ACEs and profiles of children with distinct patterns of early exposure, in a large, racially diverse cohort from the US. The authors also examine the longitudinal associations between profiles of early adversity in early childhood with later mental health and telomere length. In this commentary, we discuss key findings from the study and recommend future avenues for improving the conceptualisation of ACEs.

Gene-environment correlations and genetic confounding underlying the association between media use and mental health.

The increase in online media use and mental health problems have prompted investigations into their association, although most literature is focussed on deleterious effects. We assessed the aetiology of media use and mental health associations (M age = 22.14, SD = 0.85) using twin (n = 4000 pairs) and polygenic score methods (n = 6000 unrelated individuals) in the Twins Early Development Study. Beyond the traditionally explored negative uses of online media (online victimisation and problematic internet use), we investigate general media uses such as posting online and watching videos and distinguish both positive (pro-social behaviour) and negative (anxiety, depression, peer and behaviour problems) mental health measures. Negative media use correlated with poor mental health (r = 0.11-0.32), but general media use correlated with prosocial behaviour (r = 0.20) and fewer behavioural problems (r = - 0.24). Twin analyses showed that both general and negative media use were moderately heritable (ranging from 20 to 49%) and their associations with mental health were primarily due to genetic influences (44-88%). Genetic sensitivity analysis combining polygenic scores with heritability estimates also suggest genetic confounding. Results indicate research on the mental health impact of media use should adopt genetically informed designs to strengthen causal inference.

Childhood Maltreatment and Mental Health Problems: A Systematic Review and Meta-Analysis of Quasi-Experimental Studies.

OBJECTIVE: Childhood maltreatment is associated with mental health problems, but the extent to which this relationship is causal remains unclear. To strengthen causal inference, the authors conducted a systematic review and meta-analysis of quasi-experimental studies examining the relationship between childhood maltreatment and mental health problems. METHODS: A search of PubMed, PsycINFO, and Embase was conducted for peer-reviewed, English-language articles from database inception until January 1, 2022. Studies were included if they examined the association between childhood maltreatment and mental health problems using a quasi-experimental method (e.g., twin/sibling differences design, children of twins design, adoption design, fixed-effects design, random-intercept cross-lagged panel model, natural experiment, propensity score matching, or inverse probability weighting). RESULTS: Thirty-four quasi-experimental studies were identified, comprising 54,646 independent participants. Before quasi-experimental adjustment for confounding, childhood maltreatment was moderately associated with mental health problems (Cohen's d=0.56, 95% CI=0.41, 0.71). After quasi-experimental adjustment, a small association between childhood maltreatment and mental health problems remained (Cohen's d=0.31, 95% CI=0.24, 0.37). This adjusted association between childhood maltreatment and mental health was consistent across different quasi-experimental methods, and generalized across different psychiatric disorders. CONCLUSIONS: These findings are consistent with a small, causal contribution of childhood maltreatment to mental health problems. Furthermore, the findings suggest that part of the overall risk of mental health problems in individuals exposed to maltreatment is due to wider genetic and environmental risk factors. Therefore, preventing childhood maltreatment and addressing wider psychiatric risk factors in individuals exposed to maltreatment could help to prevent psychopathology.