To test whether adolescents who are victimized by peers are at heightened risk for suicidal ideation and suicide attempt, using both cross-sectional and prospective investigations.
Participants are ...from the Quebec Longitudinal Study of Child Development, a general population sample of children born in Quebec in 1997 through 1998 and followed up until 15 years of age. Information about victimization and serious suicidal ideation and suicide attempt in the past year was obtained at ages 13 and 15 years from self-reports (N = 1,168).
Victims reported concurrently higher rates of suicidal ideation at age 13 years (11.6-14.7%) and suicide attempt at age 15 years (5.4-6.8%) compared to those who had not been victimized (2.7-4.1% for suicidal ideation and 1.6-1.9% for suicide attempt). Being victimized by peers at 13 years predicted suicidal ideation (odds ratio OR = 2.27; 95% CI = 1.25-4.12) and suicide attempt (OR = 3.05, 95% CI = 1.36-6.82) 2 years later, even after adjusting for baseline suicidality and mental health problems and a series of confounders (socioeconomic status, intelligence, family's functioning and structure, hostile-reactive parenting, maternal lifetime suicidal ideation/suicide attempt). Those who were victimized at both 13 and 15 years had the highest risk of suicidal ideation (OR = 5.41, 95% CI = 2.53-11.53) and suicide attempt (OR = 5.85, 95% CI = 2.12-16.18) at 15 years.
Victimization is associated with an increased risk of suicidal ideation and suicide attempt over and above concurrent suicidality and prior mental health problems. The longer the history of victimization, the greater the risk.
ABSTRACT BACKGROUND Exposure to peer victimization is relatively common. However, little is known about its developmental course and its effect on impairment associated with mental illnesses. We ...aimed to identify groups of children following differential trajectories of peer victimization from ages 6 to 13 years and to examine predictive associations of these trajectories with mental health in adolescence. METHODS Participants were members of the Quebec Longitudinal Study of Child Development, a prospective cohort of 2120 children born in 1997/98 who were followed until age 15 years. We included 1363 participants with self-reported victimization from ages 6 to 13 years and data available on their mental health status at 15 years. RESULTS We identified 3 trajectories of peer victimization. The 2 prevailing groups were participants with little or moderate exposure to victimization (441/1685 26.2% and 1000/1685 59.3%, respectively); the third group (244 14.5%) had been chronically exposed to the most severe and long-lasting levels of victimization. The most severely victimized individuals had greater odds of reporting debilitating depressive or dysthymic symptoms (odds ratio OR 2.56, 95% confidence interval CI 1.27–5.17), debilitating generalized anxiety problems (OR 3.27, CI 1.64–6.51) and suicidality (OR 3.46, CI 1.53–7.81) at 15 years than those exposed to the lowest levels of victimization, after adjustment for sex, childhood mental health, family hardship and victimization perpetration. The association with suicidality remained significant after controlling for concurrent symptoms of depression or dysthymia and generalized anxiety problems. INTERPRETATION Adolescents who were most severely victimized by peers had an increased risk of experiencing severe symptoms consistent with mental health problems. Given that peer victimization trajectories are established early on, interventions to reduce the risk of being victimized should start before enrolment in the formal school system.
Using a sample of 767 children (403 girls, 364 boys), this study aimed to (a) identify groups with distinct trajectories of peer victimization over a 6-year period from primary school through the ...transition to secondary school, and (b) examine the associated personal (i.e., aggression or internalizing problems) and familial (family status, socioeconomic status, the parent-child relationship) predictors. Peer victimization was assessed via self-reports from Grades 4 through 9 (ages 10 through 15 years), aggression and internalizing problems were assessed in Grade 4 via peer nominations, and the parent-child relationship was assessed in Grade 7 (i.e., right after the transition to secondary school) via parent-reports. Growth Mixture modeling revealed 1 group (62%) who experienced little victimization in primary school and even less in secondary school, another group (31%) who was victimized in primary but not or much less in secondary school, and a third group (7%) who was chronically victimized in both school contexts. Boys were more likely than girls to follow any elevated victimization trajectory. Chronic victimization across primary and secondary school was predicted by nonintact family status and a combination of both internalizing problems and aggression compared with nonvictimized youth. In contrast, transitory victimization during primary but not in secondary school was predicted by aggression, but not internalizing problems. Support as well as conflict in the parent-child relationship also showed significant, albeit distinct associations with the different peer victimization trajectories.
Background: Research shows high co‐morbidity between gambling problems and depressive symptoms, but the directionality of this link is unclear. Moreover, the co‐occurrence of gambling problems and ...depressive symptoms could be spurious and explained by common underlying risk factors such as impulsivity and socio‐family risk. The goals of the present study were to examine 1) whether common antecedent factors explain the concurrent links between depressive symptoms and gambling problems, and 2) whether possible transactional links between depressive symptoms and gambling problems exist from late adolescence to early adulthood.
Methods: A total of 1004 males from low SES areas participated in the study.
Results: Analyses revealed a positive predictive link between impulsivity at age 14 and depressive symptoms and gambling problems at age 17. In turn, gambling problems at age 17 predicted an increase in depressive symptoms from age 17 to age 23, and depressive symptoms at age 17 predicted an increase in gambling problems from age 17 to age 23.
Conclusions: Common antecedent factors may explain the initial emergence of an association between depressive symptoms and gambling problems in adolescence. However, once emerged, their escalation seems to be better explained by a mutual direct influence between the two sets of disorders.
This study explored whether early elementary school aged children's externalizing problems impede academic functioning and foster negative social experiences such as peer victimization, thereby ...making these children vulnerable for developing internalizing problems and possibly increasing their externalizing problems. It also explored whether early internalizing problems contributed to an increase in externalizing problems. The study examined 1,558 Canadian children from ages 6 to 8 years. Externalizing and internalizing problems, peer victimization, and school achievement were assessed annually. Externalizing problems lead to academic underachievement and experiences of peer victimization. Academic underachievement and peer victimization, in turn, predicted increases in internalizing problems and in externalizing problems. These pathways applied equally to boys and girls. No links from internalizing to externalizing problems were found.
The main challenge in addressing the role of DNA methylation in human behaviour is the fact that the brain is inaccessible to epigenetic analysis in living humans. Using positron emission tomography ...(PET) measures of brain serotonin (5-HT) synthesis, we found in a longitudinal sample that adult males with high childhood-limited aggression (C-LHPA) had lower in vivo 5-HT synthesis in the orbitofrontal cortex (OBFC). Here we hypothesized that 5-HT alterations associated with childhood aggression were linked to differential DNA methylation of critical genes in the 5-HT pathway and these changes were also detectable in peripheral white blood cells. Using pyrosequencing, we determined the state of DNA methylation of SLC6A4 promoter in T cells and monocytes isolated from blood of cohort members (N = 25) who underwent a PET scan, and we examined whether methylation status in the blood is associated with in vivo brain 5-HT synthesis. Higher levels of methylation were observed in both T cells and monocytes at specific CpG sites in the C-LHPA group. DNA methylation of SLC6A4 in monocytes appears to be associated more reliably with group membership than T cells. In both cell types the methylation state of these CpGs was associated with lower in vivo measures of brain 5-HT synthesis in the left and right lateral OBFC (N = 20) where lower 5-HT synthesis in C-LHPA group was observed. Furthermore, in vitro methylation of the SLC6A4 promoter in a luciferase reporter construct suppresses its transcriptional activity supporting a functional role of DNA methylation in SLC6A4 promoter regulation. These findings indicate that state of SLC6A4 promoter methylation is altered in peripheral white blood cells of individuals with physical aggression during childhood. This supports the relevance of peripheral DNA methylation for brain function and suggests that peripheral SLC6A4 DNA methylation could be a marker of central 5-HT function.
This longitudinal study of 2,000 children revealed that inattention, but not hyperactivity, is related to whether children graduate from high school.
Objective:Literature clearly documents the ...association between mental health problems, particularly attention deficit hyperactivity disorder (ADHD), and educational attainment. However, inattention and hyperactivity are generally not considered independently from each other in prospective studies. The aim of the present study was to differentiate the unique, additive, or interactive contributions of inattention and hyperactivity symptoms to educational attainment.
Method:The authors randomly selected 2,000 participants from a representative sample of Canadian children and estimated developmental trajectories of inattention and hyperactivity between the ages of 6 and 12 years using yearly assessments. High school graduation status, at age 22–23 years, was obtained from official records.
Results:Four trajectories of inattention and four trajectories of hyperactivity were observed between the ages of 6 and 12 years. After controlling for hyperactivity and other confounding variables, a high inattention trajectory (compared with low inattention) strongly predicted not having a high school diploma at 22–23 years of age (odds ratio=7.66, 95% confidence interval CI=5.06–11.58). To a lesser extent, a declining or rising trajectory of inattention also made a significant contribution (odds ratios of 2.67 95% CI=1.90–3.75 and 3.87 95% CI=2.75–5.45, respectively). Hyperactivity was not a significant predictor once inattention was taken into account.
Conclusions:Inattention rather than hyperactivity during elementary school significantly predicts long-term educational attainment. Children with attention problems, regardless of hyperactivity, need preventive intervention early in their development.
Attention-deficit/hyperactivity disorder (ADHD) comorbid with sleep disturbances can produce profound disruption in daily life and negatively impact quality of life of both the child and the family. ...However, the temporal relationship between ADHD and sleep impairment is unclear, as are underlying common brain mechanisms.
This study used data from the Quebec Longitudinal Study of Child Development (n = 1601, 52% female) and the Adolescent Brain Cognitive Development Study (n = 3515, 48% female). Longitudinal relationships between symptoms were examined using cross-lagged panel models. Gray matter volume neural correlates were identified using linear regression. The transcriptomic signature of the identified brain-ADHD-sleep relationship was characterized by gene enrichment analysis. Confounding factors, such as stimulant drugs for ADHD and socioeconomic status, were controlled for.
ADHD symptoms contributed to sleep disturbances at one or more subsequent time points in both cohorts. Lower gray matter volumes in the middle frontal gyrus and inferior frontal gyrus, amygdala, striatum, and insula were associated with both ADHD symptoms and sleep disturbances. ADHD symptoms significantly mediated the link between these structural brain abnormalities and sleep dysregulation, and genes were differentially expressed in the implicated brain regions, including those involved in neurotransmission and circadian entrainment.
This study indicates that ADHD symptoms and sleep disturbances have common neural correlates, including structural changes of the ventral attention system and frontostriatal circuitry. Leveraging data from large datasets, these results offer new mechanistic insights into this clinically important relationship between ADHD and sleep impairment, with potential implications for neurobiological models and future therapeutic directions.
Chronic physical aggression (CPA) is characterized by frequent use of physical aggression from early childhood to adolescence. Observed in approximately 5% of males, CPA is associated with early ...childhood adverse environments and long-term negative consequences. Alterations in DNA methylation, a covalent modification of DNA that regulates genome function, have been associated with early childhood adversity.
To test the hypothesis that a trajectory of chronic physical aggression during childhood is associated with a distinct DNA methylation profile during adulthood.
We analyzed genome-wide promoter DNA methylation profiles of T cells from two groups of adult males assessed annually for frequency of physical aggression between 6 and 15 years of age: a group with CPA and a control group. Methylation profiles covering the promoter regions of 20 000 genes and 400 microRNAs were generated using MeDIP followed by hybridization to microarrays.
In total, 448 distinct gene promoters were differentially methylated in CPA. Functionally, many of these genes have previously been shown to play a role in aggression and were enriched in biological pathways affected by behavior. Their locations in the genome tended to form clusters spanning millions of bases in the genome.
This study provides evidence of clustered and genome-wide variation in promoter DNA methylation in young adults that associates with a history of chronic physical aggression from 6 to 15 years of age. However, longitudinal studies of methylation during early childhood will be necessary to determine if and how this methylation variation in T cells DNA plays a role in early development of chronic physical aggression.
High frequency of physical aggression is the central feature of severe conduct disorder and is associated with a wide range of social, mental and physical health problems. We have previously tested ...the hypothesis that differential DNA methylation signatures in peripheral T cells are associated with a chronic aggression trajectory in males. Despite the fact that sex differences appear to play a pivotal role in determining the development, magnitude and frequency of aggression, most of previous studies focused on males, so little is known about female chronic physical aggression. We therefore tested here whether or not there is a signature of physical aggression in female DNA methylation and, if there is, how it relates to the signature observed in males.
Methylation profiles were created using the method of methylated DNA immunoprecipitation (MeDIP) followed by microarray hybridization and statistical and bioinformatic analyses on T cell DNA obtained from adult women who were found to be on a chronic physical aggression trajectory (CPA) between 6 and 12 years of age compared to women who followed a normal physical aggression trajectory. We confirmed the existence of a well-defined, genome-wide signature of DNA methylation associated with chronic physical aggression in the peripheral T cells of adult females that includes many of the genes similarly associated with physical aggression in the same cell types of adult males.
This study in a small number of women presents preliminary evidence for a genome-wide variation in promoter DNA methylation that associates with CPA in women that warrant larger studies for further verification. A significant proportion of these associations were previously observed in men with CPA supporting the hypothesis that the epigenetic signature of early life aggression in females is composed of a component specific to females and another common to both males and females.
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