Background Peer victimization is ubiquitous across schools and cultures, and has been suggested as one developmental pathway to anxiety disorders. However, there is a dearth of prospective studies examining this relationship. The purpose of this cohort study was to examine the association between peer victimization during adolescence and subsequent anxiety diagnoses in adulthood. A secondary aim was to investigate whether victimization increases risk for severe anxiety presentations involving diagnostic comorbidity. Methods The sample comprised 6,208 adolescents from the Avon Longitudinal Study of Parents and Children who were interviewed about experiences of peer victimization at age 13. Maternal report of her child's victimization was also assessed. Anxiety disorders at age 18 were assessed with the Clinical Interview Schedule–Revised. Multivariable logistic regression was used to examine the association between victimization and anxiety diagnoses adjusted for potentially confounding individual and family factors. Sensitivity analyses explored whether the association was independent of diagnostic comorbidity with depression. Results Frequently victimized adolescents were two to three times more likely to develop an anxiety disorder than nonvictimized adolescents (OR = 2.49, 95% CI: 1.62–3.85). The association remained after adjustment for potentially confounding individual and family factors, and was not attributable to diagnostic overlap with depression. Frequently victimized adolescents were also more likely to develop multiple internalizing diagnoses in adulthood. Conclusions Victimized adolescents are at increased risk of anxiety disorders in later life. Interventions to reduce peer victimization and provide support for victims may be an effective strategy for reducing the burden associated with these disorders.

Young people whose parents have depression have a greatly increased risk of developing a psychiatric disorder, but poor outcomes are not inevitable. Identification of the contributors to mental health resilience in young people at high familial risk is an internationally recognised priority. Our objectives were to identify protective factors that predict sustained good mental health in adolescents with a parent with depression and to test whether these contribute beyond what is explained by parent illness severity. The Early Prediction of Adolescent Depression study (EPAD) is a prospective longitudinal study of offspring of parents with recurrent depression. Parents with recurrent major depressive disorder, co-parents, and offspring (aged 9-17 years at baseline) were assessed three times over 4 years in a community setting. Offspring outcomes were operationalised as absence of mental health disorder, subthreshold symptoms, or suicidality on all three study occasions (sustained good mental health); and better than expected mental health (mood and behavioural symptoms at follow-up lower than predicted given severity of parental depression). Family, social, cognitive, and health behaviour predictor variables were assessed using interview and questionnaire measures. Between February and June, 2007, we screened 337 families at baseline, of which 331 were eligible. Of these, 262 completed the three assessments and were included in the data for sustained mental health. Adolescent mental health problems were common, but 53 (20%) of the 262 adolescents showed sustained good mental health. Index parent positive expressed emotion (odds ratio 1·91 [95% CI 1·31-2·79]; p=0·001), co-parent support (1·90 [1·38-2·62]; p<0·0001), good-quality social relationships (2·07 [1·35-3·18]; p=0·001), self-efficacy (1·49 [1·05-2·11]; p=0·03), and frequent exercise (2·96 [1·26-6·92]; p=0·01) were associated with sustained good mental health. Analyses accounting for parent depression severity were consistent, but frequent exercise only predicted better than expected mood-related mental health (β=-0·22; p=0·0004) not behavioural mental health, whereas index parents' expression of positive emotions predicted better than expected behavioural mental health (β=-0·16; p=0·01) not mood-related mental health. Multiple protective factors were required for offspring to be free of mental health problems (zero or one protective factor, 4% sustained good mental health; two protective factors, 10%; three protective factors, 13%, four protective factors, 38%; five protective factors, 48%). Adolescent mental health problems are common, but not inevitable, even when parental depression is severe and recurrent. These findings suggest that prevention programmes will need to enhance multiple protective factors across different domains of functioning. Sir Jules Thorn Charitable Trust, Economic and Social Research Council.

Background: Elucidating risk pathways for under‐achieving at school can inform strategies to reduce the number of adolescents leaving school without passing grades in core subjects. Maternal depression can compromise the quality of parental care and is associated with multiple negative child outcomes. However, only a few small studies have investigated the association between perinatal maternal depression and poor academic achievement in adolescence. The pathways to explain the risks are also unclear. Method: Prospective observational data from 5,801 parents and adolescents taking part in a large UK population cohort (Avon‐Longitudinal‐Study‐of‐Parents‐and‐Children) were used to test associations between maternal and paternal depression and anxiety in the perinatal period, executive function ( EF ) at age 8, and academic achievement at the end of compulsory school at age 16. Results: Adolescents of postnatally depressed mothers were 1.5 times (1.19, 1.94, p = .001) as likely as adolescents of nondepressed mothers to fail to achieve a ‘pass’ grade in math; antenatal anxiety was also an independent predictor of poor math. Disruption in different components of EF explained small but significant proportions of these associations: attentional control explained 16% (4%, 27%, p < .001) of the association with postnatal depression, and working memory explained 17% (13%, 30%, p = .003) of the association with antenatal anxiety. A similar pattern was seen for language grades, but associations were confounded by maternal education. There was no evidence that paternal factors were independently associated with impaired child EF or adolescent exams. Conclusion: Maternal postnatal depression and antenatal anxiety are risk factors for adolescents underachieving in math. Preventing, identifying, and treating maternal mental health in the perinatal period could, therefore, potentially increase adolescents’ academic achievement. Different aspects of EF partially mediated these associations. Further work is needed, but if these pathways are causal, improving EF could reduce underachievement in math.

It has been suggested that prenatal maternal stress may increase the risk of childhood externalizing disorders, yet no large cohort study has investigated this association across a large range of acute stressors. Our objective was to estimate the association between prenatal stressful events and risk of offspring conduct disorder and hyperactivity. We used data from 10,184 mother-offspring pairs from the United Kingdom-based Avon Longitudinal Study of Parents and Children. Mothers self-reported 42 prenatal stressful life events at 18 weeks' gestation. Symptoms of conduct disorder and hyperactivity in their offspring were measured at 6, 9, 11, 13, and 16 years of age using the Strengths and Difficulties Questionnaire. The primary outcome was membership in high-symptom trajectories of 1) conduct disorder and 2) hyperactivity throughout childhood, identified using latent class growth modeling. Multinomial logistic regression models estimated the association between prenatal stress and both conduct disorder and hyperactivity, after adjusting for sex, parental education, low birth weight, preterm birth, parental social class, maternal smoking and drinking, maternal mental health, offspring stressful life events, and offspring depressive and anxious symptoms. Those exposed to the highest quartile of prenatal stress were more likely to belong to the high symptom trajectory for hyperactivity (B = 0.46, p < .05) and conduct disorder (B = 0.88, p < .01), respectively. Prenatal stress further demonstrated a positive, dose-response relationship with symptoms of externalizing disorders at independent time points. The findings suggest that prenatal stressful events may be an independent risk factor for offspring externalizing symptoms, regardless of maternal mental health and offspring internalizing.

The fetal programming hypothesis posits that in utero exposure to stress can alter prenatal brain development and lifelong stress response. However, human studies linking objective prenatal stressors to offspring mental illness, especially depression, are rare. The purpose of this study was to examine the association between mothers' exposure to prenatal stressful life events (SLEs) and offspring depression. The sample comprised 10,569 members of a prospective population-based cohort, the Avon Longitudinal Study of Parents and Children (ALSPAC). Mothers reported on the occurrence and impact of 42 prenatal SLEs. Offspring depressive symptoms were assessed using a computerized version of the Clinical Interview Schedule-Revised (CIS-R) at age 17 to 18, as well as 13 self-report statements from the Short Mood and Feelings Questionnaire (SMFQ) at 6 time points from ages 10 to 11 to 18 to 19. Latent class growth analysis (LCGA) was used to identify trajectories of depressive symptoms across adolescence. After adjusting for potential confounders, a 1-unit increase in maternal SLE scores (range, 0-168) during gestation was associated with increased offspring depressive symptoms (β = 0.07, p < .01) and major depression (odds ratio [OR] = 1.03, 95% CI 1.01, 1.06) at age 17 to 18. LCGA revealed 4 trajectories of depressive symptoms. High maternal SLEs (fourth quartile) were associated with membership in the trajectory characterized by stable, high levels of depression from age 10 to 11 to 18 to 19 years (OR = 1.72, 95% CI = 1.09, 2.71). These results provide support for the fetal programming hypothesis, demonstrating that prenatal exposure to acute stress is associated with offspring depression in adolescence. Stress management may be of benefit for expectant mothers.

Although childhood maltreatment is associated with long-term impairment, some children function well despite this adversity. This study aimed to identify the key protective factors for good educational attainment and positive emotional health in adolescents who experienced maltreatment in early childhood. Data were analyzed from the Avon Longitudinal Study of Parents and Children, a large UK prospective cohort study. The sample was defined by maternally reported exposure to physical or emotional maltreatment by a parent prior to 5 years. 1118 (8.0%) children were emotionally maltreated and 375 (2.7%) were physically maltreated before the age of 5. There were too few cases of sexual abuse to be considered. Positive outcomes were operationalized as achieving 5 or more grade A*-C GCSE exam grades at 16 years and scores above the cohort median on the self-report Warwick-Edinburgh Mental Wellbeing Scale and Bachmann Self-Esteem Scale at 17.5 years. The associations of individual, family and community covariates with successful adaptation to the adversity of maltreatment were investigated using logistic regression. School related factors, including engagement in extracurricular activities, satisfaction with school and not being bullied were the most important in facilitating resilience in educational attainment, self-esteem and wellbeing. Good communication and social skills was the most protective individual trait. There was insufficient evidence to suggest that family factors were associated with resilience to maltreatment. School-based interventions are recommended to promote positive adaptation following parental maltreatment. Future research should evaluate outcomes across the life-course to understand whether the protective influences of school persist into adulthood.