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Bullying victimisation has been associated with increased risk of suicide ideation and attempt throughout the lifespan, but no study has yet examined whether it translates to a greater risk of death by suicide. We aimed to determine the association of bullying victimisation with suicide mortality.
Participants were drawn from the 1958 British birth cohort, a prospective follow-up of all births in 1 week in Britain in 1958. We conducted logistic regressions on 14 946 participants whose mothers reported bullying victimisation at 7 and 11 years with linked information on suicide deaths through the National Health Service Central Register.
Fifty-five participants (48 males) had died by suicide between the age 18 and 52 years. Bullying victimisation was associated with suicide mortality; a one standard deviation increases in bullying victimisation linked to an increased odds for suicide mortality [odds ratio (OR) 1.29; 1.02–1.64] during adulthood. The OR attenuated by 11% after adjustment for individual (e.g. behavioural and emotional problems) and familial characteristics (e.g. adverse childhood experiences, 1.18; 0.92–1.51). Analysis of bullying victimisation frequency categories yields similar results: compared with individuals who had not been bullied, those who had been frequently bullied had an increased odds for suicide mortality (OR 1.89; 0.99–3.62).
Our study suggests that individuals who have been frequently bullied have a small increased risk of dying by suicide, when no other risk factors is considered. Suicide prevention might start in childhood, with bullying included in a range of inter-correlated vulnerabilities encompassing behavioural and emotional difficulties and adverse experiences within the family.
The present study examined patterns of stability and change in loneliness across adolescence. Data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a UK population-representative cohort of 2,232 individuals born in 1994 and 1995. Loneliness was assessed when participants were aged 12 and 18. Loneliness showed modest stability across these ages (r = .25). Behavioral genetic modeling indicated that stability in loneliness was explained largely by genetic influences (66%), while change was explained by nonshared environmental effects (58%). Individuals who reported loneliness at both ages were broadly similar to individuals who only reported it at age 18, with both groups at elevated risk of mental health problems, physical health risk behaviors, and education and employment difficulties. Individuals who were lonely only at age 12 generally fared better; however, they were still more likely to finish school with lower qualifications. Positive family influences in childhood predicted reduced risk of loneliness at age 12, while negative peer experiences increased the risk. Together, the findings show that while early adolescent loneliness does not appear to exert a cumulative burden when it persists, it is nonetheless a risk for a range of concomitant impairments, some of which can endure.
Peer victimization is associated with a wide range of mental health problems in youth, yet few studies described its association with mental health comorbidities.
To test the association between peer victimization timing and intensity and mental health comorbidities, we used data from 1216 participants drawn from the Quebec Longitudinal Study of Child Development, a population-based birth cohort. Peer victimization was self-reported at ages 6–17 years, and modeled as four trajectory groups: low, childhood-limited, moderate adolescence-emerging, and high-chronic. The outcomes were the number and the type of co-occurring self-reported mental health problems at age 20 years. Associations were estimated using negative binomial and multinomial logistic regression models and adjusted for parent, family, and child characteristics using propensity score inverse probability weights.
Youth in all peer victimization groups had higher rates of co-occurring mental health problems and higher likelihood of comorbid internalizing-externalizing problems [odds ratios ranged from 2.06, 95% confidence interval (CI) 1.52–2.79 for childhood-limited to 4.34, 95% CI 3.15–5.98 for high-chronic victimization] compared to those in the low victimization group. The strength of these associations was highest for the high-chronic group, followed by moderate adolescence-emerging and childhood-limited groups. All groups also presented higher likelihood of internalizing-only problems relative to the low peer victimization group.
Irrespective of timing and intensity, self-reported peer victimization was associated with mental health comorbidities in young adulthood, with the strongest associations observed for high-chronic peer victimization. Tackling peer victimization, especially when persistent over time, could play a role in reducing severe and complex mental health problems in youth.
Neurodevelopmental disorders (NDs) are associated with experiences of victimization, but mechanisms remain unclear. We explored sex differences and the role of familial factors and externalizing problems in the association between several NDs and violent victimization in adolescence and young adulthood.
Individuals born in Sweden 1985–1997, residing in Sweden at their 15th birthday, were followed until date of violent victimization causing a hospital visit or death, death due to other causes, emigration, or December 31, 2013, whichever came first. The exposures were diagnoses of attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), intellectual disability (ID) and other NDs. We used three different Cox regression models: a crude model, a model adjusted for familial confounding using sibling-comparisons, and a model additionally adjusted for externalizing problems.
Among 1 344 944 individuals followed, on average, for 5 years, 74 487 were diagnosed with NDs and 37 765 had a hospital visit or died due to violence. ADHD was associated with an increased risk of violent victimization in males [hazard ratio (HR) 2.56; 95% confidence interval (CI) 2.43–2.70) and females (HR 5.39; 95% CI 4.97–5.85). ASD and ID were associated with an increased risk of violent victimization in females only. After adjusting for familial factors and externalizing problems, only ADHD was associated with violent victimization among males (HR 1.27; 95% CI 1.06–1.51) and females (HR 1.69; 95% CI 1.21–2.36).
Females with NDs and males with ADHD are at greater risk of being victim of severe violence during adolescence and young adulthood. Relevant mechanisms include shared familial liability and externalizing problems. ADHD may be independently associated with violent victimization.
Complex traumas are traumatic experiences that involve multiple interpersonal threats during childhood or adolescence, such as repeated abuse. This type of trauma is hypothesized to lead to more severe psychopathology and poorer cognitive function than other non-complex traumas, such as road traffic accidents. However, empirical testing of this hypothesis has been limited to clinical or convenience samples and cross-sectional designs. To better understand this topic, we aimed to investigate psychopathology and cognitive function in young people exposed to complex, non-complex, or no trauma from a population-representative longitudinal cohort, and to consider the role of pre-existing vulnerabilities.
Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a population-representative birth-cohort of 2,232 children born in England and Wales in 1994-95. At age 18 years (93% participation), we assessed lifetime exposure to complex and non-complex trauma. We also assessed past-year psychopathology including general psychopathology ‘p’ and several psychiatric disorders, as well as current cognitive function including IQ, executive function, and processing speed. Additionally, we prospectively assessed early childhood vulnerabilities including internalizing and externalizing symptoms at age 5, IQ at age 5, family history of mental illness, family socioeconomic status, and sex.
We found that participants who had been exposed to complex trauma had more severe psychopathology and poorer cognitive function across wide-ranging measures at age 18, compared to both trauma-unexposed participants and those exposed to non-complex trauma. Early childhood vulnerabilities had an important role in these presentations, as they predicted risk of later complex trauma exposure, and largely explained associations of complex trauma with cognitive deficits, but not with psychopathology.
By conflating complex and non-complex traumas, current research and clinical practice under-estimate the severity of psychopathology and cognitive deficits linked with complex trauma, as well as the role of pre-existing vulnerabilities. A better understanding of the mental health needs of people exposed to complex trauma and underlying mechanisms could inform the development of new effective interventions.
Complex traumas are traumatic experiences that involve multiple interpersonal threats during childhood or adolescence, such as repeated abuse. These traumas are hypothesised to cause more severe psychopathology and poorer cognitive function than other non-complex traumas. However, empirical testing has been limited to clinical/convenience samples and cross-sectional designs.
To investigate psychopathology and cognitive function in young people exposed to complex, non-complex or no trauma, from a population-representative longitudinal cohort, and to consider the role of pre-existing vulnerabilities.
Participants were from the Environmental Risk Longitudinal Twin Study, a population-representative birth cohort of 2232 British children. At age 18 years (93% participation), we assessed lifetime exposure to complex and non-complex trauma, past-year psychopathology and current cognitive function. We also prospectively assessed early childhood vulnerabilities: internalising and externalising symptoms at 5 years of age, IQ at 5 years of age, family history of mental illness, family socioeconomic status and sex.
Participants exposed to complex trauma had more severe psychopathology and poorer cognitive function at 18 years of age, compared with both trauma-unexposed participants and those exposed to non-complex trauma. Early childhood vulnerabilities predicted risk of later complex trauma exposure, and largely explained associations of complex trauma with cognitive deficits, but not with psychopathology.
By conflating complex and non-complex traumas, current research and clinical practice underestimate the severity of psychopathology, cognitive deficits and pre-existing vulnerabilities linked with complex trauma. A better understanding of the mental health needs of people exposed to complex trauma could inform the development of new, more effective interventions.
A recent suicidal drive hypothesis posits that psychotic experiences (PEs) may serve to externalize internally generated and self-directed threat (i.e., self-injurious/suicidal behavior [SIB]) in order to optimize survival; however, it must first be demonstrated that such internal threat can both precede and inform PEs. The current study conducted the first known bidirectional analysis of SIB and PEs to test whether SIB could be considered as a plausible antecedent for PEs. Prospective data were utilized from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative birth cohort of 2232 twins, that captured SIB (any self-harm or suicidal attempt) and PEs at ages 12 and 18 years. Cross-lagged panel models demonstrated that the association between SIB at age 12 and PEs at age 18 was as strong as the association between PEs at age 12 and SIB at age 18. Indeed, the best representation of the data was a model where these paths were constrained to be equal (OR = 2.48, 95% CI = 1.63–3.79). Clinical interview case notes for those who reported both SIB and PEs at age 18, revealed that PEs were explicitly characterized by SIB/threat/death-related content for 39% of cases. These findings justify further investigation of the suicidal drive hypothesis.
The present study used a longitudinal and discordant twin design to explore in depth the developmental associations between victimization and loneliness from mid-childhood to young adulthood. The data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a birth cohort of 2,232 individuals born in England and Wales during 1994–1995. Diverse forms of victimization were considered, differing across context, perpetrator, and timing of exposure. The results indicated that exposure to different forms of victimization was associated with loneliness in a dose–response manner. In childhood, bullying victimization was uniquely associated with loneliness, over and above concurrent psychopathology, social isolation, and genetic risk. Moreover, childhood bullying victimization continued to predict loneliness in young adulthood, even in the absence of ongoing victimization. Within-twin pair analyses further indicated that this longitudinal association was explained by genetic confounds. In adolescence, varied forms of victimization were correlated with young adult loneliness, with maltreatment, neglect, and cybervictimization remaining robust to controls for genetic confounds. These findings indicate that vulnerability to loneliness in victimized young people varies according to the specific form of victimization in question, and also to the developmental period in which it was experienced.
Attention-deficit hyperactivity disorder (ADHD) is associated with poorer cognitive functioning. We used a developmental, genetically-sensitive approach to examine intelligence quotient (IQ) from early childhood to young adulthood among those with different ADHD courses to investigate whether changes in ADHD were reflected in differences in IQ. We also examined executive functioning in childhood and young adulthood among different ADHD courses.
Study participants were part of the Environmental Risk (E-Risk) Longitudinal Twin Study, a population-based birth cohort of 2232 twins. We assessed ADHD in childhood (ages 5, 7, 10 and 12) and young adulthood (age 18). We examined ADHD course as reflected by remission, persistence and late-onset. IQ was evaluated at ages 5, 12 and 18, and executive functioning at ages 5 and 18.
ADHD groups showed deficits in IQ across development compared to controls; those with persistent ADHD showed the greatest deficit, followed by remitted and late-onset. ADHD groups did not differ from controls in developmental trajectory of IQ, suggesting changes in ADHD were not reflected in IQ. All ADHD groups performed more poorly on executive functioning tasks at ages 5 and 18; persisters and remitters differed only on an inhibitory control task at age 18.
Differences in ADHD course – persistence, remission and late-onset – were not directly reflected in changes in IQ. Instead, having ADHD at any point across development was associated with lower average IQ and poorer executive functioning. Our finding that individuals with persistent ADHD have poorer response inhibition than those who remitted requires replication.
Social support has been shown to be associated with a reduced likelihood of developing psychotic experiences in the general population and even amongst those at high risk due to exposure to multiple forms of victimisation (poly-victimised). However, it is unclear whether this association is merely due to the confounding effects of shared environmental and genetic influences, or reverse causality. Therefore, we investigated whether social support has a unique environmentally mediated effect on adolescent psychotic experiences after accounting for familial factors, including genetic factors, and also prior psychopathology.
Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2232 UK-born twins. Adolescents were interviewed at age 18 about psychotic experiences and victimisation exposure since age 12, and their perceptions of social support. Prior childhood mental health problems and psychotic symptoms were assessed at age 12. The discordant twin method was used to disentangle the relative family-wide and unique-environmental effects of social support on psychotic experiences in the general population and among poly-victimised adolescents.
Perceived social support, particularly from friends, was found to have a unique environmentally mediated buffering effect on adolescent psychotic experiences in the whole sample and in the high-risk poly-victimised group.
The protective effects of social support on adolescent psychotic experiences cannot be accounted for by shared environmental or genetic factors, nor by earlier psychopathology. Our findings suggest that early intervention programmes focused on increasing perceptions of social support have the potential to prevent the emergence of psychotic experiences amongst adolescents.
Positive social relationships are known to mitigate the negative effects of stress on mental health. However, the direction of association between social resources and mental health remains unclear, and it is not known whether higher than average levels of social resources confer additional benefits, in the short and longer term.
To investigate the concurrent and longitudinal contribution of higher levels of social resources in reducing the risk of mental health symptoms after exposure to stress at age 45, and to identify life-course precursors of mid-life social resources.
The National Child Development Study (NCDS) is a prospective birth cohort of over 17 000 births in 1958. We tested concurrent and longitudinal associations between different levels of social resources at age 45 and mental health symptoms among individuals exposed to stress and verified whether prior mental health symptoms (age 42) explained these associations. We also tested a range of child, family and adult precursors of mid-life social resources.
Higher than average levels of social resources were required to confer benefits to mental health among individuals exposed to high stress levels, both concurrently at age 45 and in the longer term at age 50. In general, these associations were not attributable to prior mental health symptoms. Key predictors of mid-life social resources included evidence of early sociability.
Having a broad network of social ties and better personal support helps individuals withstand exposure to higher levels of stress. Given that sociable children had better mid-life social resources, early intervention may benefit individuals' social resources later in life.
Attention-deficit hyperactivity disorder (ADHD) is associated with mental health problems and functional impairment across many domains. However, how the longitudinal course of ADHD affects later functioning remains unclear.
We aimed to disentangle how ADHD developmental patterns are associated with young adult functioning.
The Environmental Risk (E-Risk) Longitudinal Twin Study is a population-based cohort of 2232 twins born in England and Wales in 1994–1995. We assessed ADHD in childhood at ages 5, 7, 10 and 12 years and in young adulthood at age 18 years. We examined three developmental patterns of ADHD from childhood to young adulthood – remitted, persistent and late-onset ADHD – and compared these groups with one another and with non-ADHD controls on functioning at age 18 years. We additionally tested whether group differences were attributable to childhood IQ, childhood conduct disorder or familial factors shared between twins.
Compared with individuals without ADHD, those with remitted ADHD showed poorer physical health and socioeconomic outcomes in young adulthood. Individuals with persistent or late-onset ADHD showed poorer functioning across all domains, including mental health, substance misuse, psychosocial, physical health and socioeconomic outcomes. Overall, these associations were not explained by childhood IQ, childhood conduct disorder or shared familial factors.
Long-term associations of childhood ADHD with adverse physical health and socioeconomic outcomes underscore the need for early intervention. Young adult ADHD showed stronger associations with poorer mental health, substance misuse and psychosocial outcomes, emphasising the importance of identifying and treating adults with ADHD.
The aim of this study was to build a detailed, integrative profile of the correlates of young adults’ feelings of loneliness, in terms of their current health and functioning and their childhood experiences and circumstances.
Data were drawn from the Environmental Risk Longitudinal Twin Study, a birth cohort of 2232 individuals born in England and Wales in 1994 and 1995. Loneliness was measured when participants were aged 18. Regression analyses were used to test concurrent associations between loneliness and health and functioning in young adulthood. Longitudinal analyses were conducted to examine childhood factors associated with young adult loneliness.
Lonelier young adults were more likely to experience mental health problems, to engage in physical health risk behaviours, and to use more negative strategies to cope with stress. They were less confident in their employment prospects and were more likely to be out of work. Lonelier young adults were, as children, more likely to have had mental health difficulties and to have experienced bullying and social isolation. Loneliness was evenly distributed across genders and socioeconomic backgrounds.
Young adults’ experience of loneliness co-occurs with a diverse range of problems, with potential implications for health in later life. The findings underscore the importance of early intervention to prevent lonely young adults from being trapped in loneliness as they age.
Mothers who have experienced childhood maltreatment are more likely to have children also exposed to maltreatment, a phenomenon known as intergenerational transmission. Factors in the perinatal period may contribute uniquely to this transmission, but timing effects have not been ascertained. Using structural equation modeling with 1,016 mothers and their 2,032 children in the Environmental Risk Longitudinal Twin Study, we tested the mediating role of postpartum depression between maternal childhood maltreatment and a cascade of negative child outcomes, specifically child exposure to maltreatment, internalizing symptoms, and externalizing symptoms: (a) adjusting for later maternal depression, (b) comparing across sex differences, and (c) examining the relative role of maltreatment subtypes. Mothers who had been maltreated as children, especially those who had experienced emotional or sexual abuse, were at increased risk for postpartum depression. In turn, postpartum depression predicted children’s exposure to maltreatment, followed by emotional and behavioral problems. Indirect effects from maternal childhood maltreatment to child outcomes were robust across child sex and supported significant mediation through postpartum depression; however, this appeared to be carried by mothers’ depression beyond the postpartum period. Identifying and treating postpartum depression, and preventing its recurrence, may help interrupt the intergenerational transmission of maltreatment and its sequelae.
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.
Cognitive impairment has been identified as an important aspect of major depressive disorder (MDD). We tested two theories regarding the association between MDD and cognitive functioning using data from longitudinal cohort studies. One theory, the cognitive reserve hypothesis, suggests that higher cognitive ability in childhood decreases risk of later MDD. The second, the scarring hypothesis, instead suggests that MDD leads to persistent cognitive deficits following disorder onset. We tested both theories in the Dunedin Study, a population-representative cohort followed from birth to midlife and assessed repeatedly for both cognitive functioning and psychopathology. We also used data from the Environmental Risk Longitudinal Twin Study to test whether childhood cognitive functioning predicts future MDD risk independent of family-wide and genetic risk using a discordant twin design. Contrary to both hypotheses, we found that childhood cognitive functioning did not predict future risk of MDD, nor did study members with a past history of MDD show evidence of greater cognitive decline unless MDD was accompanied by other comorbid psychiatric conditions. Our results thus suggest that low cognitive functioning is related to comorbidity, but is neither an antecedent nor an enduring consequence of MDD. Future research may benefit from considering cognitive deficits that occur during depressive episodes from a transdiagnostic perspective.
In the present study, we used separate measures of parental monitoring and parental knowledge and compared their associations with youths’ antisocial behavior during preadolescence, between the ages of 10 and 12. Parental monitoring and knowledge were reported by mothers, fathers, and youths taking part in the Environmental Risk (E-Risk) Longitudinal Twin Study that follows 1,116 families with twins. Information on youths’ antisocial behavior was obtained from mothers as well as teachers. We report two main findings. First, longitudinal cross-lagged models revealed that greater parental monitoring did not predict less antisocial behavior later, once family characteristics were taken into account. Second, greater youth antisocial behavior predicted less parental knowledge later. This effect of youths’ behavior on parents’ knowledge was consistent across mothers’, fathers’, youths’, and teachers’ reports, and robust to controls for family confounders. The association was partially genetically mediated according to a Cholesky decomposition twin model; youths’ genetically influenced antisocial behavior led to a decrease in parents’ knowledge of youths’ activities. These two findings question the assumption that greater parental monitoring can reduce preadolescents’ antisocial behavior. They also indicate that parents’ knowledge of their children's activities is influenced by youths’ behavior.
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.
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.
We report a graded relationship between neighborhood socioeconomic status (SES) and children's antisocial behavior that (a) can be observed at school entry, (b) widens across childhood, (c) remains after controlling for family-level SES and risk, and (d) is completely mediated by maternal warmth and parental monitoring (defined throughout as supportive parenting). The children were participants in the Environmental Risk Longitudinal Twin Study (N = 2,232), which prospectively tracked the development of children and their neighborhoods across childhood. Direct and independent effects of neighborhood-level SES on children's antisocial behavior were observed as early as age 5, and the gap between children living in deprived versus more affluent neighborhoods widened as children approached adolescence. By age 12, the effect of neighborhood SES on children's antisocial behavior was as large as the effect observed for our most robust predictor of antisocial behavior: sex (Cohen d = 0.51 when comparing children growing up in deprived vs. more affluent neighborhoods in comparison to Cohen d = 0.53 when comparing antisocial behavior among boys vs. girls). However, these relatively large differences in children's levels and rate of change in antisocial behavior across deprived versus more affluent neighborhoods were completely mediated by supportive parenting practices. The implications of our findings for studying and reducing socioeconomic disparities in antisocial behavior among children are discussed.