Background Evidence from animal and human studies suggests that early-life stress such as physical maltreatment has long-lasting effects on the hypothalamic-pituitary-adrenal (HPA) axis and is associated with blunted HPA axis reactivity in adulthood. Few studies have investigated whether blunted HPA axis reactivity observed in children exposed to early-life stress signals social, emotional, and behavioral problems. Methods Participants were 190 12-year-old children (50.5% males) recruited from the Environmental Risk Longitudinal Twin Study, a nationally representative 1994 to 1995 cohort of families with twins. Cortisol responses to psychosocial stress were measured in maltreated/ bullied (n = 64) and comparison children (n = 126). We ascertained maltreatment and bullying victimization using mothers’ reports and assessed children’s social, emotional, and behavioral problems at ages 5 and 12 using mothers’ and teachers’ reports. Results Piecewise multilevel growth curve analyses indicated that maltreated/bullied and comparison children showed distinct cortisol responses to stress. Specifically, maltreated/bullied children had lower cortisol responses than comparison children who exhibited a significant increase. Lower cortisol responses were, in turn, associated with more social and behavioral problems among maltreated/bullied children. Conclusions These findings provide support for the influence of childhood harm on blunted HPAaxis reactivity and its potential impacton children’s functioning. Our findings emphasize the need to integrate stress biomarkers in guiding prevention efforts for young victims.

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We investigated the antecedents and consequences of chronic victimization by bullies across a school transition using a genetically sensitive longitudinal design. Data were from the Environmental Risk Longitudinal Twin Study (E-Risk), an epidemiological cohort of 2,232 children. We used mothers’ and children’s reports of bullying victimization during primary school and early secondary school. Children who experienced frequent victimization at both time points were classed as “chronic victims” and were found to have an increased risk for mental health problems and academic difficulties compared to children who were bullied only in primary school, children bullied for the first time in secondary school, and never-bullied children. Biometric analyses revealed that stability in victimization over this period was influenced primarily by genetic and shared environmental factors. Regression analyses showed that children’s early characteristics such as preexistent adjustment difficulties and IQ predicted chronic versus transitory victimization. Family risk factors for chronic victimization included socioeconomic disadvantage, low maternal warmth, and maltreatment. Our results suggest that bullying intervention programs should consider the role of the victims’ behaviors and family background in increasing vulnerability to chronic victimization. Our study highlights the importance of widening antibullying interventions to include families to reduce the likelihood of children entering a pathway toward chronic victimization.

Background Childhood adverse experiences are known to induce persistent changes in the hypothalamic–pituitary–adrenal (HPA) axis reactivity to stress. However, the mechanisms by which these experiences shape the neuroendocrine response to stress remain unclear. Method We tested whether bullying victimization influenced serotonin transporter gene (SERT) DNA methylation using a discordant monozygotic (MZ) twin design. A subsample of 28 MZ twin pairs discordant for bullying victimization, with data on cortisol and DNA methylation, were identified in the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative 1994–1995 cohort of families with twins. Results Bullied twins had higher SERT DNA methylation at the age of 10 years compared with their non-bullied MZ co-twins. This group difference cannot be attributed to the children’s genetic makeup or their shared familial environments because of the study design. Bullied twins also showed increasing methylation levels between the age of 5 years, prior to bullying victimization, and the age of 10 years whereas no such increase was detected in non-bullied twins across time. Moreover, children with higher SERT methylation levels had blunted cortisol responses to stress. Conclusions Our study extends findings drawn from animal models, supports the hypothesis that early-life stress modifies DNA methylation at a specific cytosine–phosphate–guanine (CpG) site in the SERT promoter and HPA functioning and suggests that these two systems may be functionally associated.

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Background Theory of mind allows the understanding and prediction of other people’s behaviours based on their mental states (e.g. beliefs). It is important for healthy social relationships and thus may contribute towards children’s involvement in bullying. The present study investigated whether children involved in bullying during early adolescence had poor theory of mind in childhood. Method Participants were members of the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative sample of 2,232 children and their families. Families were visited by the authors when children were 5, 7, 10 and 12 years. Theory of mind was assessed when the children were 5 years using eight standardized tasks. Identification of those children who were involved in bullying as victims, bullies and bully-victims using mothers’, teachers’ and children’s reports was carried out when they were 12 years’ old. Results Poor theory of mind predicted becoming a victim (effect size, d=0.26), bully (d=0.25) or bully-victim (d=0.44) in early adolescence. These associations remained for victims and bully-victims when child-specific (e.g., IQ) and family factors (e.g., child maltreatment) were controlled for. Emotional and behavioural problems during middle childhood did not modify the association between poor theory of mind and adolescent bullying experiences. Conclusion Identifying and supporting children with poor theory of mind early in life could help reduce their vulnerability for involvement in bullying and thus limit its adverse effects on mental health.

Purpose To identify contextual and interpersonal factors that distinguish families in which the intergenerational transmission of maltreatment is maintained from families in which the cycle is broken. Methods The sample was composed of 1,116 families in the United Kingdom who participated in the Environmental Risk (E-Risk) Longitudinal Twin Study. We assessed mother’s childhood history of maltreatment retrospectively with a validated and reliable interview. Prospective reports of children’s physical maltreatment were collected repeatedly up to 12 years. We compared families in which mothers but not children had experienced maltreatment with families in which both mothers and children had experienced maltreatment, and with families without maltreatment, on a range of contextual and interpersonal factors known to affect child development. Results In multivariate analyses, supportive and trusting relationships with intimate partners, high levels of maternal warmth toward children, and low levels of partner violence between adults distinguished families in which mothers but not children experienced maltreatment from families in which mothers and children experienced maltreatment. Families in which only mothers experienced maltreatment were largely similar to families in which neither generation experienced maltreatment, except that mothers belonging to the former group were more likely to have a lifetime history of depression and low levels of social support. Conclusions Safe, stable, nurturing relationships between intimate partners and between mothers and children are associated with breaking the cycle of abuse in families. Additional research is needed to determine whether these factors have a causal role in preventing the transmission of maltreatment from one generation to the next.

Objective Childhood adverse experiences are known to engender persistent changes in stress-related systems and brain structures involved in mood, cognition, and behavior in animal models. Uncertainty remains about the causal effect of early stressful experiences on physiological response to stress in human beings, as the impact of these experiences has rarely been investigated while controlling for both genetic and shared environmental influences. Method We tested whether bullying victimization, a repeated adverse experience in childhood, influences cortisol responses to a psychosocial stress test (PST) using a discordant monozygotic (MZ) twin design. Thirty pairs (43.3% males) of 12-year-old MZ twins discordant for bullying victimization were identified in the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative 1994–1995 cohort of families with twins. Results Bullied and nonbullied MZ twins showed distinct patterns of cortisol secretion after the PST. Specifically, bullied twins exhibited a blunted cortisol response compared with their nonbullied MZ co-twins, who showed the expected increase. This difference in cortisol response to stress could not be attributed to children's genetic makeup, their familial environments, pre-existing and concomitant individual factors, or the perception of stress and emotional response to the PST. Conclusion Results from this natural experiment provide support for a causal effect of adverse childhood experiences on the neuroendocrine response to stress.