Youth adversity and trajectories of depression/anxiety symptoms in adolescence in the context of intersectionality in the United Kingdom.

BACKGROUND: Youth adversity is associated with persistence of depression and anxiety symptoms. This association may be greater for disadvantaged societal groups (such as females) compared with advantaged groups (e.g. males). Given that persistent symptoms are observed across a range of disadvantaged, minoritized, and neurodivergent groups (e.g. low compared with high socio-economic status [SES]), the intersection of individual characteristics may be an important moderator of inequality. METHODS: Data from HeadStart Cornwall (N = 4441) was used to assess the effect of youth adversity on combined symptoms of depression and anxiety (Strengths and Difficulties Questionnaire emotional problems subscale) measured at three time-points in 11-14-year-olds. Latent trajectories and regressions were estimated for eight intersectionality profiles (based on gender, SES, and hyperactivity/inattention), and moderating effects of the individual characteristics and their intersections were estimated. RESULTS: Youth adversity was associated with higher average depression/anxiety symptoms at baseline (11-12-years) across all intersectionality profiles. The magnitude of effects differed across profiles, with suggestive evidence for a moderating effect of youth adversity on change over time in depression/anxiety symptoms attributable to the intersection between (i) gender and SES; and (ii) gender, SES, and hyperactivity/inattention. CONCLUSIONS: The detrimental effects of youth adversity pervade across intersectionality profiles. The extent to which these effects are moderated by intersectionality is discussed in terms of operational factors. The current results provide a platform for further research, which is needed to determine the importance of intersectionality as a moderator of youth adversity on the development of depression and anxiety symptoms in adolescence.

Interplay between polygenic risk for mood disorders and stressful life events in bipolar disorder.

BACKGROUND: Although genetic and environmental factors are involved in the aetiology of bipolar disorder [BD], studies focused on their interplay are lacking. The current investigation examines interactions and correlations between polygenic risk scores [PRS] for BD and major depressive disorder [MDD] with stressful life events [SLEs] in liability for BD. METHODS: This study used data from 1715 participants (862 bipolar cases and 853 controls) taken from UK and Canadian samples. The List of Threatening Experiences Questionnaire recorded SLEs that occurred 6 months before interview for controls and 6 months prior to the first (Canadian sample) and worst (UK sample) depressive and manic episodes for bipolar cases. PRS-BD and PRS-MDD were calculated from the Psychiatric Genomics Consortium. RESULTS: For the worst depressive episode, the PRS-MDD was significantly correlated with total number of SLEs (ß = 0.13, 95 % CI:0.04-0.22, p = 0.003) and dependent SLEs (ß = 0.09, 95 % CI:0.02-0.16, p = 0.007). After correction for multiple testing nominally significant correlations were detected for PRS-BD with total number of SLEs (ß = 0.11, 95 % CI:0.02-0.20, p = 0.015) and dependent SLEs (ß = 0.08, 95 % CI:0.01-0.15, p = 0.019). Among bipolar cases, these associations were slightly stronger but were only of nominal significance for total number of SLEs (PRS-MDD: ß = 0.19, 95 % CI:0.04-0.35, p = 0.015; PRS-BD: ß = 0.16, 95 % CI:0.01-0.32, p = 0.042) and dependent SLEs (PRS-MDD: ß = 0.14, 95 % CI:0.03-0.26, p = 0.015; PRS-BD: ß = 0.12, 95 % CI:0.004-0.24, p = 0.043). No other significant gene-environment correlations or interactions were found. LIMITATIONS: Use of a larger sample size would be beneficial. CONCLUSIONS: The relationship between SLEs and genetic risk for mood disorders may be best explained through correlations rather than interactions.

Racialised staff-patient relationships in inpatient mental health wards: a realist secondary qualitative analysis of patient experience data.

BACKGROUND: The current study is a secondary analysis of qualitative data collected as part of EURIPIDES, a study which assessed how patient experience data were used to improve the quality of care in National Health Service (NHS) mental health services. OBJECTIVE: We undertook a detailed realist secondary qualitative analysis of 10 interviews in which expressions of racialisation were unexpectedly reported. This theme and these data did not form part of the primary realist evaluation. METHODS: Interviews were originally conducted with the patients (18-65 years: 40% female, 60% male) from four different geographically located NHS England mental health trusts between July and October 2017. Secondary qualitative data analysis was conducted in two phases: (1) reflexive thematic analysis and retroduction; (2) refinement of context-mechanism-outcome configurations to explore the generative mechanisms underpinning processes of racialisation and revision of the initial programme theory. FINDINGS: There were two main themes: (1) absence of safe spaces to discuss racialisation which silenced and isolated patients; (2) strained communication and power imbalances shaped a process of mutual racialisation by patients and staff. Non-reporting of racialisation and discrimination elicited emotions such as feeling othered, misunderstood, disempowered and fearful. CONCLUSIONS: The culture of silence, non-reporting and power imbalances in inpatient wards perpetuated relational racialisation and prevented authentic feedback and staff-patient rapport. CLINICAL IMPLICATIONS: Racialisation in mental health trusts reflects lack of psychological safety which weakens staff-patient rapport and has implications for authentic patient engagement in feedback and quality improvement processes. Larger-scale studies are needed to investigate racialisation in the staff-patient relationships.

Protocol for secondary data analysis of 4 UK cohorts examining youth adversity and mental health in the context of intersectionality.

BACKGROUND: Youth adversity (e.g., abuse and bullying victimisation) is robust risk factor for later mental health problems (e.g., depression and anxiety). Research shows the prevalence of youth adversity and rates of mental health problems vary by individual characteristics, identity or social groups (e.g., gender and ethnicity). However, little is known about whether the impact of youth adversity on mental health problems differ across the intersections of these characteristics (e.g., white females). This paper reports on a component of the ATTUNE research programme (work package 2) which aims to investigate the impact and mechanisms of youth adversity on depressive and anxiety symptoms in young people by intersectionality profiles. METHODS: The data are from 4 UK adolescent cohorts: HeadStart Cornwall, Oxwell, REACH, and DASH. These cohorts were assembled for adolescents living in distinct geographical locations representing coastal, suburban and urban places in the UK. Youth adversity was assessed using a series of self-report questionnaires and official records. Validated self-report instruments measured depressive and anxiety symptoms. A range of different variables were classified as possible social and cognitive mechanisms. RESULTS AND ANALYSIS: Structural equation modelling (e.g., multiple group models, latent growth models) and multilevel modelling will be used, with adaptation of methods to suit the specific available data, in accord with statistical and epidemiological conventions. DISCUSSION: The results from this research programme will broaden our understanding of the association between youth adversity and mental health, including new information about intersectionality and related mechanisms in young people in the UK. The findings will inform future research, clinical guidance, and policy to protect and promote the mental health of those most vulnerable to the negative consequences of youth adversity.

Reliability and convergent validity of retrospective reports of childhood maltreatment by individuals with bipolar disorder.

Childhood maltreatment is associated with the etiology and clinical course of bipolar disorder. Most studies employ retrospective maltreatment self-reports which are vulnerable to bias, raising questions about their validity and reliability. This study examined the test-retest reliability over 10 years, the convergent validity and the impact of current mood on retrospective reports of childhood maltreatment in a bipolar sample. 85 participants with bipolar I disorder completed the Childhood Trauma Questionnaire [CTQ] and the Parental Bonding Instrument [PBI] at baseline. Beck Depression Inventory and Self Report Mania Inventory assessed depressive and manic symptoms, respectively. 53 participants completed the CTQ at baseline and 10-year follow-up. Good levels of convergent validity were observed between the CTQ and PBI. Correlations ranged from rs= -0.35 (CTQ emotional abuse and PBI paternal care) to rs= -0.65 (CTQ emotional neglect and PBI maternal care). Good agreement between CTQ reports at baseline and 10-year follow-up were found (range: κ=0.41 for physical neglect to κ=0.83 for sexual abuse). Higher depression and mania scores were recorded among participants who reported abuse (but not neglect) compared to those without such reports. These findings support using this method in research and clinical practice, though current mood should be taken into account.

The association between childhood bullying victimisation and childhood maltreatment with the clinical expression of bipolar disorder.

Adverse childhood experiences are significantly associated with a worse clinical expression of bipolar disorder, however, the literature has mainly focused on childhood maltreatment (abuse and neglect) with little attention paid to other forms of adversity, such as childhood bullying victimisation (referred to here as bullying), although this is known to have a negative impact on different psychiatric illnesses. The current study aimed to investigate the association between bullying victimisation and the clinical expression of bipolar disorder individually and in combination with childhood maltreatment. This investigation consisted of 63 individuals with a diagnosis of bipolar disorder (mean age 61.4 years) who completed the Retrospective Bullying Questionnaire and the Childhood Trauma Questionnaire to measure exposure to bullying and childhood maltreatment, respectively. The clinical expression variables were assessed using self-report instruments, these were: the Cardiff Anomalous Perceptions Scale (psychotic symptoms), Suicide Behaviours Questionnaire, Self-Report Manic Inventory, Beck Anxiety and Depression Inventories. The results showed that exposure to bullying was significantly associated with more suicidal behaviours (F(1,61) = 11.02, p < .01, η2 = 0.15) and psychotic symptoms (F(1,61) = 4.21, p < .05, η2 = .06). When bullying and childhood maltreatment histories were combined, the results showed that individuals with a history of both adversity types reported significantly more suicidal behaviours (F(2,60) = 6.59, p < .01, R2=.18) compared to those with a history of one or neither form of adversity. The sample size, age and gender distribution, limit the generalisability of the findings. However, the current results underscore the need to account for bullying victimisation when considering the adverse childhood experiences-bipolar disorder relationship, especially its clinical expression.

Intergenerational Continuity of Intimate Partner Violence Perpetration: An Investigation of Possible Mechanisms.

Intimate partner violence (IPV) is a continuum of abuse that is associated with a number of negative outcomes including substance misuse, depression, and suicidal ideation. This study aims to investigate the intergenerational transmission of IPV perpetration and the mechanisms involved. Intergenerational transmission was investigated using information from two generations of the Cambridge Study in Delinquent Development which is a prospective longitudinal study of 411 males from an inner London area in the UK who have been followed up over a period of 50 years. Information with regard to IPV perpetration, specifically physical violence, was garnered from self-reports by the male at age 32, from their female partner at age 48, and from their male and female children in early adulthood. Regression analyses were used to investigate intergenerational transmission and examine whether psychosocial risk factors could be identified as potential intergenerational pathways. Having a father who was a perpetrator of IPV significantly increased the odds of daughters being perpetrators by 2 times. It did not significantly increase the odds for sons. The intergenerational transmission of IPV perpetration remains between fathers and their daughters over and above a series of psychosocial factors such as accommodation problems and alcohol misuse. Identification of factors associated with the intergenerational transmission of IPV perpetration will inform practitioners and policymakers. Information garnered from studies such as this may contribute to the development of prevention and intervention strategies for those at risk.

Bullying behaviours and other conduct problems: longitudinal investigation of their independent associations with risk factors and later outcomes.

PURPOSE: Bullying behaviours and other conduct problems often co-occur. However, we do not yet know whether bullying behaviours are associated with early factors and later poor outcomes independently of conduct problems. While there are differing, specific interventions for bullying behaviours and for conduct problems, it is unclear if such specificity is justified given parallels between both behaviours. METHODS: We used prospective data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative sample of 2232 children. Mothers and teachers reported on children's bullying behaviours and conduct problems at ages 7 and 10. We collected measures of risk factors, including temperament and family factors, when children were age 5. We assessed behavioural, emotional, educational and social problems when participants reached the ages of 12 and 18. RESULTS: Bullying behaviours and conduct problems co-occurred in childhood. Our findings indicated that bullying behaviours and other conduct problems were independently associated with the same risk factors. Furthermore, they were associated with the same poor outcomes at both ages 12 and 18. Despite this, bullying behaviours were uniquely associated with behavioural, emotional, educational and social problems at age 18. CONCLUSIONS: Our findings suggest that anti-bullying programmes and interventions aimed at reducing conduct problems could benefit from greater integration. Furthermore, our study highlights the mental health problems children who bully may face in later years and the need to consider those in intervention plans.

The association between bullying-victimisation and sleep disturbances in adolescence: Evidence from a twin study.

Bullying-victimisation has been associated with sleep disturbances. This study investigated the degree to which subtypes of bullying-victimisation in adolescence are linked with sleep disturbances. Genetic and environmental contributions underlying bullying-victimisation and sleep disturbances were investigated. Participants (3,242-5,076 pairs) from a longitudinal community twin study reported on their bullying-victimisation at the age of 14 years, and sleep quality and insomnia symptoms at age 16. Regression analyses were used, accounting for the role of individual and family factors. Structural equation twin model fitting was conducted. Bullying-victimisation was modestly associated with sleep quality and insomnia symptoms (r = 0.22-0.23) and a similar strength of associations was found across bullying-victimisation subtypes (r = 0.11-0.22). Bullying-victimisation, sleep quality and insomnia symptoms were predominantly influenced by genes (25-59%) and non-shared environments (40-62%). The association between bullying-victimisation and sleep quality was explained by genetic and non-shared environmental influences. For insomnia symptoms and sleep quality, the association with bullying-victimisation was in part explained by a genetic overlap. Associations between bullying-victimisation and sleep disturbances are not limited to specific aspects of bullying-victimisation but appear to exist for all subtypes. These findings stimulate research questions regarding the mechanisms underlying these links. For example, could certain heritable traits, such as temperament, increase vulnerability to experiencing sleep disturbances and being bullied? Research on bullying and sleep should aim to take the role of genetic predisposition into account, while also noting that it is not the only causal influence. Understanding more about these pathways could strengthen the development of techniques to prevent these difficulties from occurring.

A twin study exploring the association between childhood emotional and behaviour problems and specific psychotic experiences in a community sample of adolescents.

BACKGROUND: Childhood emotional and behaviour problems are antecedents for later psychopathology. This study investigated genetic and environmental influences shaping the longitudinal association between childhood emotional and behaviour problems and specific PEs. METHOD: In a community-based twin sample, parents reported on emotional and behaviour problems when twins were ages 7 and 12 years. At age 16 years, specific PEs were measured using self-reports and parent reports. Structural equation model-fitting was conducted. RESULTS: Childhood emotional and behaviour problems were significantly associated with paranoia, cognitive disorganisation and parent-rated negative symptoms in adolescence (mean r = .15-.38), and to a lesser extent with hallucinations, grandiosity and anhedonia (mean r = .04-.12). Genetic influences on childhood emotional and behaviour problems explained significant proportions of variance in adolescent paranoia (4%), cognitive disorganisation (8%) and parent-rated negative symptoms (3%). Unique environmental influences on childhood emotional and behaviour problems explained ≤1% of variance in PEs. Common environmental influences were only relevant for the relationship between childhood emotional and behaviour problems and parent-rated negative symptoms (explaining 28% of variance) and are partly due to correlated rater effects. CONCLUSIONS: Childhood emotional and behaviour problems are significantly, if weakly, associated with adolescent PEs. These associations are driven in part by common genetic influences underlying both emotional and behaviour problems and PEs. However, psychotic experiences in adolescence are largely influenced by genetic and environmental factors that are independent of general childhood emotional and behaviour problems, suggesting they are not merely an extension of childhood emotional and behaviour problems.

Association between stressful life events and psychotic experiences in adolescence: evidence for gene-environment correlations.

BACKGROUND: Stressful life events (SLEs) are associated with psychotic experiences. SLEs might act as an environmental risk factor, but may also share a genetic propensity with psychotic experiences. AIMS: To estimate the extent to which genetic and environmental factors influence the relationship between SLEs and psychotic experiences. METHOD: Self- and parent reports from a community-based twin sample (4830 16-year-old pairs) were analysed using structural equation model fitting. RESULTS: SLEs correlated with positive psychotic experiences (r = 0.12-0.14, all P<0.001). Modest heritability was shown for psychotic experiences (25-57%) and dependent SLEs (32%). Genetic influences explained the majority of the modest covariation between dependent SLEs and paranoia and cognitive disorganisation (bivariate heritabilities 74-86%). The relationship between SLEs and hallucinations and grandiosity was explained by both genetic and common environmental effects. CONCLUSIONS: Further to dependent SLEs being an environmental risk factor, individuals may have an underlying genetic propensity increasing their risk of dependent SLEs and positive psychotic experiences.

Psychotic experiences are linked to cannabis use in adolescents in the community because of common underlying environmental risk factors.

Cannabis users are more likely to have psychotic experiences (PEs). The degree to which these associations are driven by genetic or environmental influences in adolescence is unknown. This study estimated the genetic and environmental contributions to the relationship between cannabis use and PEs. Specific PEs were measured in a community-based twin sample (4830 16-year-old pairs) using self-reports and parent-reports. Adolescents reported on ever using cannabis. Multivariate liability threshold structural equation model-fitting was conducted. Cannabis use was significantly correlated with PEs. Modest heritability (37%), common environmental influences (55%) and unique environment (8%) were found for cannabis use. For PEs, modest heritability (27-54%), unique environmental influences (E=12-50%) and little common environmental influences (11-20%), with the exception of parent-rated Negative Symptoms (42%), were reported. Environmental influences explained all of the covariation between cannabis use and paranoia, cognitive disorganization and parent-rated negative symptoms (bivariate common environment=69-100%, bivariate unique environment=28-31%), whilst the relationship between cannabis use and hallucinations indicated familial influences. Cannabis use explains 2-5% of variance in positive, cognitive, and negative PEs. Cannabis use and psychotic experience co-occur due to environmental factors. Focus on specific environments may reveal why adolescent cannabis use and psychotic experiences tend to 'travel together'.

A shared genetic propensity underlies experiences of bullying victimization in late childhood and self-rated paranoid thinking in adolescence.

BACKGROUND: Bullying is a risk factor for developing psychotic experiences (PEs). Whether bullying is associated with particular PEs, and the extent to which genes and environments influence the association, are unknown. This study investigated which specific PEs in adolescence are associated with earlier bullying victimization and the genetic and environmental contributions underlying their association. METHOD: Participants were 4826 twin pairs from a longitudinal community-based twin study in England and Wales who reported on their bullying victimization at the age of 12 years. Measures of specific PEs (self-rated Paranoia, Hallucinations, Cognitive disorganization, Grandiosity, Anhedonia, and parent-rated Negative Symptoms) were recorded at age of 16 years. RESULTS: Childhood bullying victimization was most strongly associated with Paranoia in adolescence (r = .26; P < .01), with weaker associations with Hallucinations, Cognitive Disorganization, parent-rated Negative Symptoms (r = .12-.20; P < .01), Grandiosity (r = .04; P < .05), and Anhedonia (r = .00, n.s.). Bivariate twin model-fitting demonstrated that bullying victimization and Paranoia were both heritable (35% and 52%, respectively) with unique environmental influences (39% and 48%, respectively), and bullying victimization showed common environmental influences (26%). The association between bullying victimization and Paranoia operated almost entirely via genetic influences (bivariate heritability = 93%), with considerable genetic overlap (genetic correlation = .55). CONCLUSION: In contrast to the assumed role of bullying victimization as an environmental trigger, these data suggest that bullying victimization in late childhood is particularly linked to self-rated Paranoia in adolescence via a shared genetic propensity. Clinically, individuals with a history of bullying victimization are predicted to be particularly susceptible to paranoid symptoms.

Chronic bullying victimization across school transitions: the role of genetic and environmental influences.

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.

A prospective longitudinal study of children's theory of mind and adolescent involvement in bullying.

BACKGROUND: Theory of mind (ToM) 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 ToM 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. We visited families when children were 5, 7, 10 and 12 years. ToM 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 ToM 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 ToM and adolescent bullying experiences. CONCLUSION: Identifying and supporting children with poor ToM early in life could help reduce their vulnerability for involvement in bullying and thus limit its adverse effects on mental health.

Blunted cortisol responses to stress signal social and behavioral problems among maltreated/bullied 12-year-old children.

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 HPA axis reactivity and its potential impact on children's functioning. Our findings emphasize the need to integrate stress biomarkers in guiding prevention efforts for young victims.

A discordant monozygotic twin design shows blunted cortisol reactivity among bullied children.

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.

Mothers and children as informants of bullying victimization: results from an epidemiological cohort of children.

Stressful events early in life can affect children's mental health problems. Collecting valid and reliable information about children's bad experiences is important for research and clinical purposes. This study aimed to (1) investigate whether mothers and children provide valid reports of bullying victimization, (2) examine the inter-rater reliability between the two informants, (3) test the predictive validity of their reports with children's emotional and behavioral problems and (4) compare the genetic and environmental etiology of bullying victimization as reported by mothers and children. We assessed bullying victimization in the Environmental-Risk (E-Risk) Longitudinal Twin Study, a nationally-representative sample of 1,116 families with twins. We collected reports from mothers and children during private interviews, including detailed narratives. Findings showed that we can rely on mothers and children as informants of bullying victimization: both informants provided information which adhered to the definition of bullying as involving repeated hurtful actions between peers in the presence of a power imbalance. Although mothers and children modestly agreed with each other about who was bullied during primary and secondary school, reports of bullying victimization from both informants were similarly associated with children's emotional and behavioral problems and provided similar estimates of genetic and environmental influences. Findings from this study suggest that collecting information from multiple informants is ideal to capture all instances of bullying victimization. However, in the absence of child self-reports, mothers can be considered as a viable alternative, and vice versa.

Health-related quality of life in a clinical sample of obese children and adolescents.

BACKGROUND: Obesity affects ethnic minority groups disproportionately, especially in the pediatric population. However, little is known about the impact of obesity on health-related quality of life (HRQoL) in children and adolescents from mixed-ethnic samples. The purpose of this study was to: 1) measure HRQoL in a mixed-ethnic clinical sample of obese children and adolescents, 2) compare HRQoL assessments in obese participants and healthy controls, and 3) compare HRQoL in obese children and adolescents according to their pubertal status. METHODS: A clinical sample of children and adolescents with obesity (n = 96) and healthy children and adolescents attending local schools (n = 444) completed the Pediatric Quality of Life Inventory (PedsQL; UK version 4). Age-appropriate versions were self-administered by children and adolescents aged 8-18 years, and interview administered to children aged 5-7 years. Multiple regression analyses controlling for age, gender, pubertal status, and ethnicity were used to compare the PedsQL scores of the two samples. RESULTS: The clinical sample of obese children and adolescents had poorer HRQoL scores on all dimensions of the PedsQL compared to the healthy controls (p < 0.005). Subsequent analyses also demonstrated that in this sample of mixed-ethnic children and adolescents, prepubescent obese children achieved the poorest scores in the emotional functioning dimension. CONCLUSIONS: Obesity significantly impacts on physical, emotional, social and school functioning of mixed-ethnic children and adolescents. Clinicians need to be aware of the significant impact of obesity on all aspects of functioning. More effort is required to target interventions to improve the quality of life of children with obesity.