The role of fathers in child development from preconception to postnatal influences: Opportunities for the National Institutes of Health Environmental influences on Child Health Outcomes (ECHO) program.

A growing body of literature highlights the important role of paternal health and socioemotional characteristics in child development, from preconception through adolescence. Much of this research addresses the indirect effects of fathers, for instance, their influence on maternal behaviors during the prenatal period or via the relationship with their partner. However, emerging evidence also recognizes the direct role of paternal health and behavior for child health and adjustment across development. This critical review presents evidence of biological and sociocultural influences of fathers on preconception, prenatal, and postnatal contributions to child development. The National Institutes of Health Environmental influences on Child Health Outcomes (ECHO) program incorporates in its central conceptualization the impact of fathers on family and child outcomes. This critical synthesis of the literature focuses on three specific child outcomes in the ECHO program: health outcomes (e.g., obesity), neurodevelopmental outcomes (e.g., emotional, behavioral, psychopathological development), and positive health. We highlight the unique insights gained from the literature to date and provide next steps for future studies on paternal influences.

Cross-cohort change in parent-reported emotional problem trajectories across childhood and adolescence in the UK.

BACKGROUND: Over the past three decades, the prevalence of adolescent emotional problems (ie, anxiety and depression) has risen. Although the onset and developmental course of emotional symptoms shows high variability, no study has directly tested secular differences across development. Our aim was to investigate whether and how developmental trajectories of emotional problems have changed across generations. METHODS: We used data from two UK prospective cohorts assessed 10 years apart: the Avon Longitudinal Study of Parents and Children (ALSPAC) including individuals born in 1991-92, and the Millennium Cohort Study (MCS) with individuals born in 2000-02. Our outcome was emotional problems, assessed using the parent-rated emotional subscale of the Strengths and Difficulties Questionnaire (SDQ-E) at approximate ages 4, 7, 8, 10, 11, 13, and 17 years in ALSPAC and ages 3, 5, 7, 11, 14, and 17 years in MCS. Participants were included if the SDQ-E was completed at least once in childhood and at least once in adolescence. Trajectories were generated using multilevel growth curve models using the repeated assessments of the SDQ-E in children aged 3-17 years. FINDINGS: Data were available for 19 418 participants (7012 from ALSPAC and 12 406 from the MCS), of whom 9678 (49·8%) were female and 9740 (50·2%) were male, and 17 572 (90·5%) had White mothers. Individuals born between 2000 and 2002 had higher emotional problem scores from around 9 years (intercept statistic ß 1·75, 95% CI 1·71-1·79) than did individuals born in 1991-92 (1·55, 1·51-1·59). The later cohort had an earlier onset of problems than the earlier cohort, and sustained higher average trajectories from around 11 years, with female adolescents showing the steepest trajectories of emotional problems. Differences between cohorts peaked overall at age 14 years. INTERPRETATION: Our comparison of two cohorts of young people provides evidence that compared with a cohort assessed 10 years prior, emotional problems emerge earlier in development in the more recent cohort, and these are especially pronounced for females during mid-adolescence. Such findings have implications for public health planning and service provision. FUNDING: Wolfson Centre for Young People's Mental Health, Wolfson Foundation.

Life satisfaction and mental health from age 17 to 21 years in a general population sample.

Adolescence is a period when both mental health (MH) and wellbeing start deteriorating, which raises the question of how the two phenomena are linked and whether deterioration in one might be used to flag problematic developments in the other. While research shows that wellbeing and MH are associated, the direction of the association is not clear and longitudinal analyses, that might help disentangle the cause and effect, are scarce. Moreover, few studies have investigated the directional relation between MH and wellbeing early in the life course. In emerging adulthood, evidence indicates reciprocal associations and no gender differences, whereas, in early and middle adolescence, results are mixed and differ across gender. Thus, we investigated the relationship between MH and wellbeing and the moderating effect of gender in the crucial developmental transition from middle adolescence to emerging adulthood. We undertake a cross-lagged longitudinal data analysis from a pooled sample of six pseudo-cohorts, including information from 661 young people who participated in the UK Household Longitudinal Study at ages 17, 19, and 21. Using a 7-points overall life satisfaction (LS) scale as an index of wellbeing and the 12-item General Health Questionnaire as a measure of MH, we found no associations between LS and MH in the 17-19 transition and bidirectional associations in the 19-21 transition. There were no substantial gender differences in either transition. We conclude that LS and MH predict each other in the transition from late adolescence (age 19) to emerging adulthood (age 21) for both males and females.

Using genetic designs to identify likely causal environmental contributions to psychopathology.

The multifactorial nature of psychopathology, whereby both genetic and environmental factors contribute risk, has long been established. In this paper, we provide an update on genetically informative designs that are utilized to disentangle genetic and environmental contributions to psychopathology. We provide a brief reminder of quantitative behavioral genetic research designs that have been used to identify potentially causal environmental processes, accounting for genetic contributions. We also provide an overview of recent molecular genetic approaches that utilize genome-wide association study data which are increasingly being applied to questions relevant to psychopathology research. While genetically informative designs typically have been applied to investigate the origins of psychopathology, we highlight how these approaches can also be used to elucidate potential causal environmental processes that contribute to developmental course and outcomes. We highlight the need to use genetically sensitive designs that align with intervention and prevention science efforts, by considering strengths-based environments to investigate how positive environments can mitigate risk and promote children's strengths.

Genetic Liabilities Differentiating Bipolar Disorder, Schizophrenia, and Major Depressive Disorder, and Phenotypic Heterogeneity in Bipolar Disorder.

Importance: Understanding the origins of clinical heterogeneity in bipolar disorder (BD) will inform new approaches to stratification and studies of underlying mechanisms. Objective: To identify components of genetic liability that are shared between BD, schizophrenia, and major depressive disorder (MDD) and those that differentiate each disorder from the others and to examine associations between heterogeneity for key BD symptoms and each component. Design, Setting, and Participants: Using data from the Bipolar Disorder Research Network in the United Kingdom, components of liability were identified by applying genomic structural equation modeling to genome-wide association studies of schizophrenia, BD, and MDD. Polygenic risk scores (PRS) representing each component were tested for association with symptoms in an independent BD data set. Adults with DSM-IV BD or schizoaffective disorder, bipolar type, were included. Data were collected from January 2000 to December 2013, and data were analyzed from June 2020 to February 2022. Main Outcomes and Measures: PRS representing the components of liability were tested for association with mania and depression, psychosis, and mood incongruence of psychosis in participants with BD, measured using the Bipolar Affective Disorder Dimensional Scale. Results: Of 4429 included participants, 3012 (68.0%) were female, and the mean (SD) age was 46.2 (12.3) years. Mania and psychosis were associated with the shared liability component (mania ß = 0.29; 95% CI, 0.23-0.34; P = 3.04 × 10-25; psychosis ß = 0.05; 95% CI, 0.04-0.07; P = 2.33 × 10-13) and the components that differentiate each of schizophrenia (mania ß = 0.08; 95% CI, 0.03-0.14; P = .002; psychosis ß = 0.03; 95% CI, 0.01-0.04; P = 1.0 × 10-4) and BD (mania ß = 0.14; 95% CI, 0.09-0.20; P = 1.99 × 10-7; psychosis ß = 0.02; 95% CI, 0.01-0.03; P = .006) from the other disorders. The BD differentiating component was associated with mania independently of effects on psychosis (ß = 0.14; 95% CI, 0.08-0.20; P = 4.32 × 10-6) but not with psychosis independently of mania. Conversely, the schizophrenia differentiating component was associated with psychosis independently of effects on mania (ß = 0.01; 95% CI, 0.003-0.03; P = .02), but not with mania independently of psychosis. Mood incongruence of psychosis was associated only with the schizophrenia differentiating component (ß = 0.03; 95% CI, 0.01-0.05; P = .005). Depression was associated with higher MDD differentiating component (ß = 0.07; 95% CI, 0.01-0.12; P = .01) but lower BD differentiating component (ß = -0.11; 95% CI, -0.17 to -0.06; P = 7.06 × 10-5). Conclusions and Relevance: In this study of BD, clinical heterogeneity reflected the burden of liability to BD and the contribution of alleles that have differentiating effects on risk for other disorders; mania, psychosis, and depression were associated with the components of genetic liability differentiating BD, MDD, and schizophrenia, respectively. Understanding the basis of this etiological heterogeneity will be critical for identifying the different pathophysiological processes underlying BD, stratifying patients, and developing precision therapeutics.

Examining the Role of Genetic Risk and Longitudinal Transmission Processes Underlying Maternal Parenting and Psychopathology and Children's ADHD Symptoms and Aggression: Utilizing the Advantages of a Prospective Adoption Design.

Although genetic factors may contribute to initial liability for ADHD onset, there is growing evidence of the potential importance of the rearing environment on the developmental course of ADHD symptomatology. However, associations between family-level variables (maternal hostility, maternal depressive symptoms) and child behaviors (developmental course of ADHD and aggression) may be explained by genes that are shared by biologically related parents and children. Furthermore, ADHD symptoms and aggression commonly co-occur: it is important to consider both simultaneously to have a better understanding of processes underlying the developmental course of ADHD and aggression. To addresses these issues, we employed a longitudinal genetically sensitive parent-offspring adoption design. Analyses were conducted using Cohort I (n = 340) of the Early Growth and Development Study with cross-validation analyses conducted with Cohort II (n = 178). Adoptive mother hostility, but not depression, was associated with later child ADHD symptoms and aggression. Mothers and their adopted children were genetically unrelated, removing passive rGE as a possible explanation. Early child impulsivity/activation was associated with later ADHD symptoms and aggression. Child impulsivity/activation was also associated with maternal hostility, with some evidence for evocative gene-environment correlation processes on adoptive mother depressive symptoms. This study provides novel insights into family-based environmental influences on child ADHD and aggression symptoms, independent of shared parental genetic factors, implications of which are further explicated in the discussion.

Using a cross-cohort comparison design to test the role of maternal smoking in pregnancy in child mental health and learning: evidence from two UK cohorts born four decades apart.

BACKGROUND: Maternal smoking in pregnancy is associated with low birth weight (LBW), child conduct problems, hyperactivity and lower cognitive attainment, but associations may reflect measured and unmeasured confounding. Cross-cohort designs can aid causal inference through comparison of associations across populations with different confounding structures. We compared associations between maternal smoking in pregnancy and child conduct and hyperactivity problems, cognition and LBW across two cohorts born four decades apart. METHODS: Two national UK cohorts born in 1958 (n = 12 415) and 2000/01 (n = 11 800) were compared. Maternal smoking in pregnancy and child birth weight was assessed at or shortly after birth. Parents rated children's conduct problems and hyperactivity, and children completed standardized tests of reading and mathematics. RESULTS: Maternal smoking in pregnancy was less common and more strongly associated with social disadvantage in 2000/01 compared with 1958 (interactions P < 0.001). Maternal smoking in pregnancy was robustly and equivalently associated with infant LBW in both cohorts [interactions: boys odds ratio (OR) = 1.01 (0.89, 1.16), P = 0.838; girls OR = 1.01 (0.91, 1.17), P = 0.633]. Maternal smoking was more strongly associated with conduct problems, hyperactivity and reading in the 2000/01 cohort (interactions P < 0.001). CONCLUSIONS: Marked cross-cohort change in associations between maternal smoking and child conduct problems, hyperactivity and reading highlights the likely role of confounding factors. In contrast, association with LBW was unaffected by change in prevalence of maternal smoking and patterns of confounding. The study highlights the utility of cross-cohort designs in helping triangulate conclusions about the role of putative causal risk factors in observational epidemiology.

Cross-cohort change in adolescent outcomes for children with mental health problems.

BACKGROUND: Child mental health problems are common. Previous studies have examined secular changes in their prevalence but have not assessed whether later outcomes have changed. We therefore aimed to test whether outcomes of child mental health problems have changed over a 40-year period. METHODS: Three cohorts were utilized: The National Child Development Study (NCDS: N = 14,544, aged 7 in 1965), the Avon Longitudinal Study of Parents and Children (ALSPAC: N = 8,188, aged 7 in 1998), and the Millennium Cohort Study (MCS: N = 13,192, aged 7 in 2008). Mental health problems at age 7 were identified using the parent-reported Rutter-A scale (NCDS) and Strengths and Difficulties Questionnaire (ALSPAC and MCS). Associated outcomes were compared across cohorts: age 11 social functioning, age 16 exam attainment and age 16 mental health. RESULTS: Child mental health problems were common in each cohort (boys: 7.0%-9.7%; girls: 5.4%-8.4%). Child mental health problems became more strongly associated with social functioning problems (boys: NCDS OR = 1.95 (1.50, 2.53), MCS OR = 3.77 (2.89, 4.92); interaction p < .001; girls: NCDS OR = 1.69 (1.22, 2.33), MCS OR = 3.99 (3.04, 5.25), interaction p < .001), lower academic attainment for boys (NCDS OR = 0.49 (0.31, 0.78), ALSPAC OR = 0.30 (0.22, 0.41), interaction p = .009), and age 16 mental health problems (boys: NCDS d' = 0.55 (0.38, 0.72), ALSPAC d' = 0.95 (0.73, 1.16); interaction p = .004; girls: NCDS d' = 0.50 (0.34, 0.65), ALSPAC d' = 0.99 (0.78, 1.20); interaction p < .001). CONCLUSIONS: Child mental health problems have become more strongly associated with negative social, educational and mental health outcomes in recent generations.

Brief report: a comparison of child mental health inequalities in three UK population cohorts.

There are substantial health disparities between children from low and higher income families. The study aimed to test changes in child mental health inequalities across three large UK population cohorts of 11-year-old children assessed in 1999, 2004 and 2012 as part of the British Child and Adolescent Mental Health Surveys and Millennium Cohort Study. Child mental health was assessed using parent and teacher versions of the Strengths and Difficulties Questionnaire. There were substantial differences in parent and teacher reported symptom scores between children from low and higher income families in each cohort. Differences in parent-reported symptoms increased over time (ES 0.35 [95% CI 0.20, 0.49] in 1999, ES 0.39 [95% CI 0.17, 0.61] in 2004, ES 0.54 [95% CI 0.49, 0.58] in 2012); cohort interaction: p = 0.01). This study found that marked child mental health inequalities exist. The mental health gap between advantaged and disadvantaged children has not reduced over the last 20 years and may be getting worse.

Associations between schizophrenia genetic risk, anxiety disorders and manic/hypomanic episode in a longitudinal population cohort study.

BACKGROUND: Studies involving clinically recruited samples show that genetic liability to schizophrenia overlaps with that for several psychiatric disorders including bipolar disorder, major depression and, in a population study, anxiety disorder and negative symptoms in adolescence.AimsWe examined whether, at a population level, association between schizophrenia liability and anxiety disorders continues into adulthood, for specific anxiety disorders and as a group. We explored in an epidemiologically based cohort the nature of adult psychopathology sharing liability to schizophrenia. METHOD: Schizophrenia polygenic risk scores (PRSs) were calculated for 590 European-descent individuals from the Christchurch Health and Development Study. Logistic regression was used to examine associations between schizophrenia PRS and four anxiety disorders (social phobia, specific phobia, panic disorder and generalised anxiety disorder), schizophrenia/schizophreniform disorder, manic/hypomanic episode, alcohol dependence, major depression, and - using linear regression - total number of anxiety disorders. A novel population-level association with hypomania was tested in a UK birth cohort (Avon Longitudinal Study of Parents and Children). RESULTS: Schizophrenia PRS was associated with total number of anxiety disorders and with generalised anxiety disorder and panic disorder. We show a novel population-level association between schizophrenia PRS and manic/hypomanic episode. CONCLUSIONS: The relationship between schizophrenia liability and anxiety disorders is not restricted to psychopathology in adolescence but is present in adulthood and specifically linked to generalised anxiety disorder and panic disorder. We suggest that the association between schizophrenia liability and hypomanic/manic episodes found in clinical samples may not be due to bias.Declarations of interestNone.

Resilience in high-risk adolescents of mothers with recurrent depressive disorder: The contribution of fathers.

This study examines the role of paternal emotional support as a resilience promoter in offspring of mothers with depression by considering the role of fathers' mental health and the quality of the couple relationship. Two hundred and sixty-five mothers with recurrent unipolar depression, partners and adolescents from Wales were assessed. Paternal emotional support, couple relationship quality, and paternal depression were assessed at baseline; adolescent mental health symptoms were assessed using the Child and Adolescent Psychiatric Assessment at follow-up. Results showed evidence of an indirect pathway whereby couple relationship quality predicted paternal emotional support (ß = -.21, 95% CI [-.34, -.08]; p = .002) which in turn predicted adolescent depression (ß = -.18, 95% CI [-.33, -.04]; p = .02), but not disruptive behaviours (ß = -.08, 95% CI [-.22, .07]; p = .30), after controlling for relevant confounders. The findings highlight that fathers and the broader family system play an important role in enhancing resilience to depression symptoms in at-risk adolescents.

Annual Research Review: Interparental conflict and youth psychopathology: an evidence review and practice focused update.

The quality of the interparental relationship is recognized as an important influence on child and adolescent psychopathology. Historically, clinically oriented research on this topic has focused on the impacts of parental divorce and domestic violence as primary interparental relationship influences on child outcomes, to the relative neglect of dimensional or qualitative features of the couple/interparental relationship for youth (child and adolescent) psychopathology. Recent research has highlighted that children are affected by attributes of interparental conflict, specifically how parents express and manage conflicts in their relationship, across a continuum of expressed severity and negativity - ranging from silence to violence. Furthermore, new evidence highlights that children's emotional, behavioral, social, academic outcomes, and future interpersonal relationships are adversely affected by conflict between parents/carers whether adults are living together or not (i.e. married or separated), or where children are or are not genetically related to their rearing parents (e.g. adoption). We review evidence and present an integrated theoretical model, highlighting how children are affected by interparental conflict and what this evidence base means for effective intervention and prevention program development, as well as the development of possible cost-benefit models. Additionally, we review policy implications of this research and highlight some very recent examples of UK-based policy focusing on addressing the interparental relationship and its impact on youth psychopathology.

How Can Genetically Informed Research Help Inform the Next Generation of Interparental and Parenting Interventions?

There is robust evidence that the interparental relationship and parenting behaviors each have a significant influence on children's risk for emotional (internalizing) and behavioral (externalizing) problems. Indeed, interventions targeting the interparental relationship and parenting processes show significant intervention-related reductions in child internalizing and externalizing problems. However, most evidence-based parenting- and couple-focused interventions result in small to medium effects on children's emotional and behavior problems. It is proposed that there is opportunity to improve upon these interventions through incorporation of knowledge from quantitative genetic research. Three core recommendations are provided for practitioners engaging in intervention work with children and families. These recommendations are contextualized relative to what quantitative genetic studies can tell us about the role of the interparental relationship and parenting behaviors on child outcomes.

Antecedents of New-Onset Major Depressive Disorder in Children and Adolescents at High Familial Risk.

Importance: Early-onset major depressive disorder (MDD) is common in individuals at high familial risk of depression and is associated with poor long-term mental health, social, and educational outcomes. Objectives: To examine the developmental pathways that lead to first-episode adolescent-onset MDD (incident cases) in those at high familial risk and to postulate a theoretically informed model that enables simultaneous testing of different pathways to incident adolescent-onset MDD composed of contributions from familial/genetic and social risk factors, as well as effects via specific clinical antecedents. Design, Setting, and Participants: This investigation was a 4-year longitudinal study (April 2007 to March 2011) among offspring of depressed parents in the general community. Analyses were conducted between September 1, 2015, and May 27, 2016. Participants were 337 families in whom the index parent (315 mothers and 22 fathers) had experienced at least 2 episodes of MDD (recruited through primary care) and among whom there was a biologically related child in the age range of 9 to 17 years living with the index parent (197 girls and 140 boys with a mean [SD] age of 12.4 [2.0] years) at baseline. Offspring with MDD before the study or at baseline (n = 27), offspring with an episode of MDD that had remitted by follow-up (n = 4), and offspring with missing baseline MDD data (n = 2) were excluded. Ninety-two percent (279 of 304) of families completed the follow-up. Main Outcomes and Measures: The primary outcome was new-onset offspring MDD, and the secondary outcome was the total DSM-IV MDD symptom score. Results: On average, children and adolescents had a mean (SD) of 1.85 (1.74) (range, 0-8.5) DSM-IV symptoms of MDD at follow-up. Twenty (6 males and 14 females) had new-onset MDD, with a mean (SD) age at onset of 14.4 (2.0) years (range, 10-18 years). Irritability (ß = 0.12, P = .03) and fear and/or anxiety (ß = 0.38, P < .001) were significant independent clinical antecedents of new adolescent-onset MDD, but disruptive behavior (ß = -0.08, P = .14) and low mood (ß = -0.03, P = .65) were not. The results were similar for the DSM-IV symptom count at follow-up. All the measured familial/genetic and social risk indicators directly influenced risk for new-onset MDD rather than indirectly through acting on dimensional clinical antecedents. Conclusions and Relevance: There are multiple pathways to first-onset adolescent depression in individuals at familial risk. Irritability and fear/anxiety may be additional clinical phenomena to be included as targets in primary preventive interventions focusing on the child. In addition to targeting these phenomena in parents and children, depression prevention methods in high-risk groups may need to take into consideration social risks, such as poverty and psychosocial adversity.

Identifying key parent-reported symptoms for detecting depression in high risk adolescents.

Adolescent offspring of depressed parents are at particularly heightened risk of developing early onset Major Depressive Disorder (MDD) yet are unlikely to access services. We therefore aimed to identify a parsimonious combination of parent-reported symptoms that accurately detected offspring MDD. We used a multi-sample study comprising a development sample of 335 offspring of adults with recurrent MDD assessed on three occasions (mean age 12.4-14.8 years) and an independent validation sub-sample of 807 adolescents from a general population cohort (mean age 13.1 years). Parent ratings of psychiatric symptoms in adolescent offspring were assessed using established questionnaires. The best performing four-item combination of symptoms was identified. Accuracy in detecting concurrent DSM-IV MDD diagnosis, assessed by direct adolescent and parent interviews, was compared to the well-established 13-item short Moods and Feelings Questionnaire (sMFQ) using ROC curve analysis. The combination identified (concentration problems, anhedonia, worrying excessively and feeling unloved) performed equivalently to the sMFQ both in the development dataset and in the validation dataset. We concluded that a combination of four parent-reported mental health items performs equivalently to an established, longer depression questionnaire measure in detecting a diagnosis of adolescent major depressive disorder among offspring of parents with recurrent MDD and needs further evaluation.

Examining whether offspring psychopathology influences illness course in mothers with recurrent depression using a high-risk longitudinal sample.

Depression is known to be influenced by psychosocial stressors. For mothers with recurrent depressive illness, the presence of psychopathology in their children may have important effects on their own mental health. Although the impact of maternal depression on child mental health is well-established, no study to date, as far as we are aware, has examined the extent to which offspring psychopathology influences the course of depression in mothers with a history of recurrent depressive illness, what types of child psychopathology impact maternal mental health, or whether risks vary by child gender. Aims were to (a) Use a longitudinal design to examine whether adolescent psychopathology (depression, disruptive behavior disorder; DBD) predicts recurrence of a depressive episode and depression symptom course in women with a history of recurrent depression; and (b) To test if observed effects vary by child gender. 299 mothers with recurrent major depressive disorder and their adolescent offspring were assessed on 2 occasions, 29 months apart. Maternal depression and offspring psychopathology were assessed using semistructured interview measures. Cross-generational links across time were assessed using structural equation modeling. Analyses were adjusted for past severity of maternal depression. Offspring depression symptoms but not DBD symptoms at baseline predicted future episode recurrence in mothers. Depression symptoms in daughters (ß = .16, p = .039) but not sons (ß = -.07, p = .461), predicted an increase in maternal depression symptoms across time. Psychopathology in daughters is associated with long-term depressive symptoms in women (mothers) with a history of recurrent depression. Findings highlight the importance of careful assessment and management of mental health problems in adolescents for more effective management of maternal depression. This study suggests that offspring symptoms of depression may be important for the recurrence of maternal depression episodes. Girls' symptoms of depression may be a particularly important psychosocial stressor for the development of depressive symptoms in mothers with a history of recurrent depression.

Mental health resilience in the adolescent offspring of parents with depression: a prospective longitudinal study.

BACKGROUND: 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. METHODS: 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. FINDINGS: 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 (ß=-0·22; p=0·0004) not behavioural mental health, whereas index parents' expression of positive emotions predicted better than expected behavioural mental health (ß=-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%). INTERPRETATION: 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. FUNDING: Sir Jules Thorn Charitable Trust, Economic and Social Research Council.

Higher cognitive ability buffers stress-related depressive symptoms in adolescent girls.

Stress has been shown to have a causal effect on risk for depression. We investigated the role of cognitive ability as a moderator of the effect of stressful life events on depressive symptoms and whether this varied by gender. Data were analyzed in two adolescent data sets: one representative community sample aged 11-12 years (n = 460) and one at increased familial risk of depression aged 9-17 years (n = 335). In both data sets, a three-way interaction was found whereby for girls, but not boys, higher cognitive ability buffered the association between stress and greater depressive symptoms. The interaction was replicated when the outcome was a diagnosis of major depressive disorder. This buffering effect in girls was not attributable to coping efficacy. However, a small proportion of the variance was accounted for by sensitivity to environmental stressors. Results suggest that this moderating effect of cognitive ability in girls is largely attributable to greater available resources for cognitive operations that offer protection against stress-induced reductions in cognitive processing and cognitive control which in turn reduces the likelihood of depressive symptomatology.