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Highlights • Childhood victimization predicted elevated levels of CRP at age 18. • The association between child victimization and CRP levels was specific to females. • Latent genetic influences on CRP levels did not explain the association in females., 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 18 years as part of the Environmental Risk (E-Risk) Longitudinal Twin Study. Childhood victimization was measured prospectively from birth to age 12 years. Inflammation was measured through C-reactive protein (CRP) levels in dried blood spots at age 18 years. 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.

Objective: Victimized adolescents have elevated risk of self-injurious thoughts and behaviors. However, poor understanding of causal and non-causal mechanisms underlying this observed risk limits the development of interventions to prevent premature death among adolescents. We tested whether pre-existing family-wide and individual vulnerabilities account for victimized adolescents’ elevated risk of self-injurious thoughts and behaviors. Method: Participants were 2,232 British children followed from birth to age 18 as part of the Environmental Risk (E-Risk) Longitudinal Twin Study. Adolescent victimization (maltreatment, neglect, sexual victimization, family violence, peer/sibling victimization, cyber-victimization, and crime victimization) was assessed through interviews with participants and co-informant questionnaires at the age 18 assessment. Suicidal ideation, self-harm, and suicide attempt in adolescence were assessed through interviews with participants at age 18. Results: Victimized adolescents had an increased risk of suicidal ideation (Odds Ratio [OR]= 2.40, 95% CI=2.11-2.74), self-harm (OR=2.38, 95% CI=2.10-2.69), and suicide attempt (OR=3.14, 95% CI=2.54-3.88). Co-twin control and propensity-score matching analyses showed that these associations were largely accounted for pre-existing familial and individual vulnerabilities, respectively. Over and above their prior vulnerabilities, victimized adolescents still showed a modest elevation in risk for suicidal ideation (OR=1.36, 95%CI=1.06-1.76) and self-harm (OR=1.50, 95% CI=1.18-1.91), but not suicide attempt (OR=1.28, 95% CI=0.83-1.98). Conclusions: Risk for self-injurious thoughts and behaviors in victimized adolescents is only partly explained by the experience of victimization. Pre-existing vulnerabilities account for a large proportion of the risk. Therefore, effective interventions to prevent premature death in victimized adolescents should not only target the experience of victimization but also address pre-existing vulnerabilities.

ObjectiveWe tested whether children who are socially isolated early in their schooling develop mental health problems in early adolescence, taking into account their mental health and family risk at school entry.MethodWe used data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a birth cohort of 2,232 children born in England and Wales in 1994 and 1995. We measured social isolation using mothers’ and teachers’ reports at ages 5 and 12. We assessed mental health symptoms via mothers’ and teachers’ ratings at age 5 and self-report measures at age 12.We collected mother-reported information about the family environment when children were 5 years old. We conducted regression analyses to test concurrent and longitudinal associations between early family factors, social isolation, and mental health difficulties.ResultsAt both primary and secondary school, children who were socially isolated experienced greater mental health difficulties. Children with behavioral problems or attention-deficit/hyperactivity disorder (ADHD) symptoms at age 5 had an elevated risk of becoming more socially isolated at age 12. However, children who were isolated at age 5 did not have greater mental health symptoms at age 12, over and above pre-existing difficulties.ConclusionAlthough social isolation and mental health problems co-occur in childhood, early isolation does not predict worse mental health problems later on. However, children who exhibit problematic behaviors may struggle to cope with the social challenges that accompany their progression through the early school years.

Endothelial dysfunction predicts mortality but it is unknown whether childhood obesity predicts adult endothelial dysfunction. The aim of this study was to determine whether anthropometric indices of body fat in childhood, adolescence and early midlife are associated with endothelial dysfunction in early midlife.Participants belonged to a representative birth cohort of 1037 individuals born in Dunedin, New Zealand in 1972 and 1973 and followed to age 38 years, with 95% retention (the Dunedin Multidisciplinary Health and Development Study). We assessed anthropometric indices of obesity at ages 3, 5, 7, 9, 11, 13, 15, 18, 21, 26, 32 and 38 years. We tested associations between endothelial function assessed by peripheral arterial tonometry (PAT) at age 38 and; age 38 cardiovascular risk factors; age 3 body mass index (BMI); and four BMI trajectory groups from childhood to early midlife.Early midlife endothelial dysfunction was associated with BMI, large waist circumference, low high-density lipoprotein cholesterol, low cardiorespiratory fitness and increased high-sensitivity C-reactive protein. After adjustment for sex and childhood socioeconomic status, 3-year-olds with BMI 1 s.d. above the mean had Framingham-reactive hyperemia index (F-RHI) ratios that were 0.10 below those with normal BMI (β=-0.10, 95% confidence interval (CI) -0.17 to -0.03, P=0.007) at age 38. Cohort members in the 'overweight', 'obese' and 'morbidly obese' trajectories had F-RHI ratios that were 0.08 (β=-0.08, 95% CI -0.14 to -0.03, P=0.003), 0.13 (β=-0.13, 95% CI -0.21 to -0.06, P0.001) and 0.17 (β=-0.17, 95% CI -0.33 to -0.01, P=0.033), respectively, below age-peers in the 'normal' trajectory.Childhood BMI and the trajectories of BMI from childhood to early midlife predict endothelial dysfunction evaluated by PAT in early midlife.

This paper presents multilevel findings on adolescents' victimization exposure from a large longitudinal cohort of twins. Data were obtained from the Environmental Risk (E-Risk) Longitudinal Twin Study, an epidemiological study of 2,232 children (1,116 twin pairs) followed to 18 years of age (with 93% retention). To assess adolescent victimization, we combined best practices in survey research on victimization with optimal approaches to measuring life stress and traumatic experiences, and introduce a reliable system for coding severity of victimization. One in three children experienced at least one type of severe victimization during adolescence (crime victimization, peer/sibling victimization, Internet/mobile phone victimization, sexual victimization, family violence, maltreatment, or neglect), and most types of victimization were more prevalent among children from low socioeconomic backgrounds. Exposure to multiple victimization types was common, as was revictimization; over half of those physically maltreated in childhood were also exposed to severe physical violence in adolescence. Biometric twin analyses revealed that environmental factors had the greatest influence on most types of victimization, while severe physical maltreatment from caregivers during adolescence was predominantly influenced by heritable factors. The findings from this study showcase how distinct levels of victimization measurement can be harmonized in large-scale studies of health and development.

Table S1. The top-ranked DMPs (P

Table S1. The top-ranked DMPs (P

Asthma is the most common chronic inflammatory disorder in children. The etiology of asthma pathology is complex and highly heterogeneous, involving the interplay between genetic and environmental risk factors that is hypothesized to involve epigenetic processes. Our aim was to explore whether methylomic variation in early childhood is associated with discordance for asthma symptoms within monozygotic (MZ) twin-pairs recruited from the Environmental Risk (E-Risk) longitudinal twin study. We also aimed to identify differences in DNA methylation that are associated with asthma that develops in childhood and persists into early adulthood as these may represent useful prognostic biomarkers.