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Background: Children with developmental language disorder (DLD) experience higher levels of peer victimization than their peers. However, it is not known if such associations reflect genetic and environmental confounding. We used a co‐twin control design to investigate the association of language difficulties (DLD and separately poor pragmatic language) with peer victimization and compare the developmental trajectories of peer victimization across adolescence for those with and without language difficulties. Methods: Participants were 3,400 pairs of twins in the Twins Early Development Study (TEDS), a UK‐based population birth cohort. Language abilities were assessed via online tests at age 11 and peer victimization was self‐reported at ages 11, 14 and 16. Language difficulties were defined as language abilities at least −1.25 SD below the mean of the TEDS sample. We performed linear regressions and latent growth curve modeling at a population level and within monozygotic and same‐sex dizygotic twin pairs. Results: At population level, youth with DLD experienced higher levels of peer victimization at ages 11 (β = 0.27, 95% Confidence Interval (CI) 0.20–0.35), 14 (β = 0.15, 95% CI 0.03–0.27) and 16 (β = 0.17, 95% CI 0.03–0.32) and a sharper decline in peer victimization between ages 11 and 16 compared to their peers without DLD. The associations between DLD and peer victimization were reduced in strength and not statistically significant in within‐twin models. Moreover, there was no difference in the rate of change in peer victimization between twin pairs discordant for DLD. Results were similar for the association of poor pragmatic language with peer victimization. Conclusions: Associations between language difficulties (DLD and separately, poor pragmatic language) and peer victimization were confounded by genetic and shared environmental factors. Identifying specific factors underlying these associations is important for guiding future work to reduce peer victimization among adolescents with language difficulties. [ABSTRACT FROM AUTHOR]

Background Identifying causal risk factors for self-harm is essential to inform preventive interventions. Epidemiological studies have identified risk factors associated with self-harm, but these associations can be subject to confounding. By implementing genetically informed methods to better account for confounding, this study aimed to better identify plausible causal risk factors for self-harm. Methods and findings Using summary statistics from 24 genome-wide association studies (GWASs) comprising 16,067 to 322,154 individuals, polygenic scores (PSs) were generated to index 24 possible individual risk factors for self-harm (i.e., mental health vulnerabilities, substance use, cognitive traits, personality traits, and physical traits) among a subset of UK Biobank participants (N = 125,925, 56.2% female) who completed an online mental health questionnaire in the period from 13 July 2016 to 27 July 2017. In total, 5,520 (4.4%) of these participants reported having self-harmed in their lifetime. In binomial regression models, PSs indexing 6 risk factors (major depressive disorder [MDD], attention deficit/hyperactivity disorder [ADHD], bipolar disorder, schizophrenia, alcohol dependence disorder, and lifetime cannabis use) predicted self-harm, with effect sizes ranging from odds ratio (OR) = 1.05 (95% CI 1.02 to 1.07, q = 0.008) for lifetime cannabis use to OR = 1.20 (95% CI 1.16 to 1.23, q = 1.33 x 10.sup.-35) for MDD. No systematic differences emerged between suicidal and non-suicidal self-harm. To further probe causal relationships, two-sample Mendelian randomisation (MR) analyses were conducted, with MDD, ADHD, and schizophrenia emerging as the most plausible causal risk factors for self-harm. The genetic liabilities for MDD and schizophrenia were associated with self-harm independently of diagnosis and medication. Main limitations include the lack of representativeness of the UK Biobank sample, that self-harm was self-reported, and the limited power of some of the included GWASs, potentially leading to possible type II error. Conclusions In addition to confirming the role of MDD, we demonstrate that ADHD and schizophrenia likely play a role in the aetiology of self-harm using multivariate genetic designs for causal inference. Among the many individual risk factors we simultaneously considered, our findings suggest that systematic detection and treatment of core psychiatric symptoms, including psychotic and impulsivity symptoms, may be beneficial among people at risk for self-harm., Author(s): Kai Xiang Lim 1, Frühling Rijsdijk 1, Saskia P. Hagenaars 1, Adam Socrates 1, Shing Wan Choi 1,2, Jonathan R. I. Coleman 1, Kylie P. Glanville 1, Cathryn M. [...]

Objective: The disruption caused by the COVID‐19 pandemic has been associated with poor mental health, including increases in eating disorders and self‐harm symptoms. We investigated risk and protective factors for the new onset of these symptoms during the pandemic. Method: Data were from the COVID‐19 Psychiatry and Neurological Genetics study and the Repeated Assessment of Mental health in Pandemics Study (n = 36,715). Exposures were socio‐demographic characteristics, lifetime psychiatric disorder, and COVID‐related variables, including SARS‐CoV‐2 infection/illness with COVID‐19. We identified four subsamples of participants without pre‐pandemic experience of our outcomes: binge eating (n = 24,211), low weight (n = 24,364), suicidal and/or self‐harm ideation (n = 18,040), and self‐harm (n = 29,948). Participants reported on our outcomes at frequent intervals (fortnightly to monthly). We fitted multiple logistic regression models to identify factors associated with the new onset of our outcomes. Results: Within each subsample, new onset was reported by: 21% for binge eating, 10.8% for low weight, 23.5% for suicidal and/or self‐harm ideation, and 3.5% for self‐harm. Shared risk factors included having a lifetime psychiatric disorder, not being in paid employment, higher pandemic worry scores, and being racially minoritized. Conversely, infection with SARS‐CoV‐2/illness with COVID‐19 was linked to lower odds of binge eating, low weight, and suicidal and/or self‐harm ideation. Discussion: Overall, we detected shared risk factors that may drive the comorbidity between eating disorders and self‐harm. Subgroups of individuals with these risk factors may require more frequent monitoring during future pandemics. Public Significance: In a sample of 35,000 UK residents, people who had a psychiatric disorder, identified as being part of a racially minoritized group, were not in paid employment, or were more worried about the pandemic were more likely to experience binge eating, low weight, suicidal and/or self‐harm ideation, and self‐harm for the first time during the pandemic. People with these risk factors may need particular attention during future pandemics to enable early identification of new psychiatric symptoms. [ABSTRACT FROM AUTHOR]

Background: Self-harm is a major health concern, not only as a signal of distress but also as a strong predictor of later suicide. Self-harm can be further refined into suicidal self-harm (SSH, i.e. suicide attempt) and non-suicidal self-harm (NSSH). Understanding the aetiologies of NSSH and SSH can help inform suicide prevention strategies. Using a twin design, we investigated the phenotypic and aetiological relationships between NSSH and SSH, and their aetiological overlap with mental health problems. Methods: We analysed data from the Twins Early Development Study using structural equation modelling. At age 21 years, 9063 twins (62.4% female) answered questions related to self-harm. At age 16 years, 19 self- or parent-reported mental health measures were administered, including measures of internalising and externalising problems, psychotic-like experiences and substance abuse. Results: Prevalences for NSSH and SSH were 21.9% and 10.5%, respectively. Additive genetic factors explained half of the variance in NSSH (55%) and SSH (50%), with the rest explained by non-shared environmental factors. Phenotypically, NSSH and SSH were strongly correlated (r = 0.87) with their correlation explained by genetic (57%) and non-shared environmental (43%) factors. We found no evidence that NSSH and SSH differed in their phenotypic and aetiological relationships with mental health measures. Conclusion: Our findings suggest no aetiological difference between NSSH and SSH. NSSH and SSH should be regarded as two different ends of a continuum, rather than as two distinct categories. [ABSTRACT FROM AUTHOR]

Background: Attention-deficit/hyperactivity disorder (ADHD) and body mass index (BMI) are associated. However, it remains unclear whether this association reflects causal relationships in either direction or confounding. Here, we implemented genetically informed methods to examine bidirectional causality and potential confounding.Methods: Three genetically informed methods were employed: (i) cross-lagged twin-differences analyses to assess bidirectional effects of ADHD symptoms and BMI at ages 8, 12, 14 and 16 years in 2386 pairs of monozygotic twins from the Twins Early Development Study (TEDS); (ii) within- and between-family ADHD and BMI polygenic score (PS) analyses in 3320 pairs of dizygotic TEDS twins; and (iii) two-sample bidirectional Mendelian randomization (MR) using summary statistics from genome-wide association studies (GWAS) on ADHD (N = 55,374) and BMI (N = 806,834).Results: Mixed results were obtained across the three methods. Twin-difference analyses provided little support for cross-lagged associations between ADHD symptoms and BMI over time. PS analyses were consistent with bidirectional relationships between ADHD and BMI, with plausible time-varying effects from childhood to adolescence. MR findings also suggested bidirectional causal effects between ADHD and BMI. Multivariable MR indicated the presence of substantial confounding in bidirectional relationships.Conclusions: The three methods converged to highlight multiple sources of confounding in the association between ADHD and BMI. PS and MR analyses suggested plausible causal relationships in both directions. Possible explanations for mixed causal findings across methods are discussed. [ABSTRACT FROM AUTHOR]

Background: Traumatic experiences are described as the strongest predictors of major depressive disorder (MDD), with inflammation potentially mediating the association between trauma and symptom onset. However, several studies indicate that body mass index (BMI) exerts a large confounding effect on both inflammation and MDD., Methods: First, we sought to replicate previously reported associations between these traits in a large subset of the UK Biobank, using regression models with C-reactive protein (CRP) and MDD and as the outcome variables in 113,481 and 30,137 individuals, respectively. Second, we ran bidirectional Mendelian randomization analyses between these traits to establish a potential causal framework between BMI, MDD, reported childhood trauma, and inflammation., Results: Our phenotypic analyses revealed no association between CRP and MDD but did suggest a strong effect of BMI and reported trauma on both CRP (BMI: β = 0.43, 95% CI = 0.43-0.43, p ≤ .001; childhood trauma: β = 0.02, 95% CI = 0.00-0.03, p  = .006) and MDD (BMI: odds ratio [OR] = 1.16, 95% CI = 1.14-1.19, p ≤ .001; childhood trauma: OR = 1.99, 95% CI = 1.88-2.11, p ≤ .001). Our Mendelian randomization analyses confirmed a lack of causal relationship between CRP and MDD but showed evidence consistent with a strong causal influence of higher BMI on increased CRP (β = 0.37, 95% CI = 0.36-0.39, p ≤ .001) and a bidirectional influence between reported trauma and MDD (OR trauma-MDD = 1.75, 95% CI = 1.49-2.07, p ≤ .001; OR MDD-trauma = 1.22, 95% CI = 1.18-1.27, p ≤ .001)., Conclusions: Our findings highlight the importance of controlling for both BMI and trauma when studying MDD in the context of inflammation. They also suggest that the experience of traumatic events can increase the risk for MDD and that MDD can increase the experience of traumatic events., (© 2022 The Authors.)