Stratifying early-onset emotional disorders: using genetics to assess persistence in young people of European and South Asian ancestry.

BACKGROUND: Depression and anxiety are the most common mental health problems in young people. Currently, clinicians are advised to wait before initiating treatment for young people with these disorders as many spontaneously remit. However, others develop recurrent disorder but this subgroup cannot be identified at the outset. We examined whether psychiatric polygenic scores (PGS) could help inform stratification efforts to predict those at higher risk of recurrence. METHODS: Probable emotional disorder was examined in two UK population cohorts using the emotional symptoms subscale of the Strengths and Difficulties Questionnaire (SDQ). Those with emotional disorder at two or more time points between ages 5 and 25 years were classed as 'recurrent emotional disorder' (n = 1,643) and those with emotional disorder at one time point as having 'single episode emotional disorder' (n = 1,435, controls n = 8,715). We first examined the relationship between psychiatric PGS and emotional disorders in childhood and adolescence. Second, we tested whether psychiatric PGS added to predictor variables of known association with emotional disorder (neurodevelopmental comorbidity, special educational needs, family history of depression and socioeconomic status) when discriminating between single-episode and recurrent emotional disorder. Analyses were conducted separately in individuals of European and South Asian ancestry. RESULTS: Probable emotional disorder was associated with higher PGS for major depressive disorder (MDD), anxiety, broad depression, ADHD and autism spectrum disorder (ASD) in those of European ancestry. Higher MDD and broad depression PGS were associated with emotional disorder in people of South Asian ancestry. Recurrent, compared to single-episode, emotional disorder was associated with ASD and parental psychiatric history. PGS were not associated with episode recurrence, and PGS did not improve discrimination of recurrence when combined with clinical predictors. CONCLUSIONS: Our findings do not support the use of PGS as a tool to assess the likelihood of recurrence in young people experiencing their first episode of emotional disorder.

Trends in adolescent emotional problems in Wales between 2013 and 2019: the contribution of peer relationships.

BACKGROUND: Epidemiological evidence shows a substantial increase in adolescent emotional problems in many countries, but reasons for this increase remain poorly understood. We tested change in emotional problems in a national sample of young people in Wales in 2013, 2017 and 2019 using identical symptom screens, and examined whether trends were accounted for by changes in youth friendship quality and bullying. METHODS: The present study of 230,735 11-16-year olds draws on repeat cross-sectional data obtained on three occasions (2013, 2017 and 2019) in national school-based surveys in Wales (conducted by the School Health Research Network). Emotional problems were assessed with a brief validated symptom screen (the SCL-4). RESULTS: There was a significant increase in emotional problem scores between 2013 and 2019 (b[95% CI] = 1.573 [1.380, 1.765]). This increase was observed for all ages and was more pronounced for girls than boys (interaction b [95% CI] = 0.229 [0.004, 0.462]) and for young people from less affluent families (interaction b [95% CI] = -0.564[-0.809, -0.319]). Of the total sample, 14.2% and 5.7% reported frequent face-to-face and cyberbullying respectively. There were modest decreases in friendship quality and increases in rates of bullying between 2013 and 2019, but accounting for these changes did not attenuate estimates of the population-level increase in emotional problems. CONCLUSIONS: This study provides evidence of a substantial increase in emotional problems among young people in Wales, particularly for young people from less affluent backgrounds. Changes in bullying or friendship quality did not explain this increase.

Developing and validating a prediction model of adolescent major depressive disorder in the offspring of depressed parents.

BACKGROUND: Parental depression is common and is a major risk factor for depression in adolescents. Early identification of adolescents at elevated risk of developing major depressive disorder (MDD) in this group could improve early access to preventive interventions. METHODS: Using longitudinal data from 337 adolescents at high familial risk of depression, we developed a risk prediction model for adolescent MDD. The model was externally validated in an independent cohort of 1,384 adolescents at high familial risk. We assessed predictors at baseline and MDD at follow-up (a median of 2-3 years later). We compared the risk prediction model to a simple comparison model based on screening for depressive symptoms. Decision curve analysis was used to identify which model-predicted risk score thresholds were associated with the greatest clinical benefit. RESULTS: The MDD risk prediction model discriminated between those adolescents who did and did not develop MDD in the development (C-statistic = .783, IQR (interquartile range) = .779, .778) and the validation samples (C-statistic = .722, IQR = -.694, .741). Calibration in the validation sample was good to excellent (calibration intercept = .011, C-slope = .851). The MDD risk prediction model was superior to the simple comparison model where discrimination was no better than chance (C-statistic = .544, IQR = .536, .572). Decision curve analysis found that the highest clinical utility was at the lowest risk score thresholds (0.01-0.05). CONCLUSIONS: The developed risk prediction model successfully discriminated adolescents who developed MDD from those who did not. In practice, this model could be further developed with user involvement into a tool to target individuals for low-intensity, selective preventive intervention.

Maternal caregiving moderates the impact of antenatal maternal cortisol on infant stress regulation.

BACKGROUND: Emerging evidence suggests that antenatal exposure to maternal stress signals affects the development of the infant stress response systems. Animal studies indicate that maternal sensitive caregiving can reverse some of these effects. However, the generalizability of these findings to humans is unknown. This study investigated the role of maternal caregiving in the association between multiple markers of maternal antenatal stress and infant stress regulation. METHODS: The sample consisted of 94 mother-infant (N = 47 males, mean postnatal weeks = 12; SD = 1.84) dyads. Maternal levels of Interleukin-6, C-Reactive Protein (CRP), diurnal cortisol and alpha amylase, depressive and anxiety symptoms were assessed in late pregnancy (mean gestational age = 34.76; SD = 1.12), whereas postnatal symptomatology, caregiving, and infant cortisol response to the inoculation were evaluated at 3 months. RESULTS: Hierarchical linear models (HLMs) showed a significant interaction between maternal antenatal cortisol, caregiving, and time on infant cortisol reactivity, while controlling for gender, maternal age, and postnatal depression. Specifically, higher levels of maternal antenatal cortisol were associated with greater cortisol response only among infants of less emotionally available mothers. All other markers of antenatal stress were not significantly associated with infant cortisol reactivity either independently or in interaction with maternal caregiving. CONCLUSIONS: Albeit preliminary, results provide the first evidence in humans that maternal sensitive caregiving may eliminate the association between antenatal maternal cortisol and infant cortisol regulation.

ADHD and depression: investigating a causal explanation.

BACKGROUND: Attention-deficit hyperactivity disorder (ADHD) is associated with later depression and there is considerable genetic overlap between them. This study investigated if ADHD and ADHD genetic liability are causally related to depression using two different methods. METHODS: First, a longitudinal population cohort design was used to assess the association between childhood ADHD (age 7 years) and recurrent depression in young-adulthood (age 18-25 years) in N = 8310 individuals in the Avon Longitudinal Study of Parents and Children (ALSPAC). Second, two-sample Mendelian randomization (MR) analyses examined relationships between genetic liability for ADHD and depression utilising published Genome-Wide Association Study (GWAS) data. RESULTS: Childhood ADHD was associated with an increased risk of recurrent depression in young-adulthood (OR 1.35, 95% CI 1.05-1.73). MR analyses suggested a causal effect of ADHD genetic liability on major depression (OR 1.21, 95% CI 1.12-1.31). MR findings using a broader definition of depression differed, showing a weak influence on depression (OR 1.07, 95% CI 1.02-1.13). CONCLUSIONS: Our findings suggest that ADHD increases the risk of depression later in life and are consistent with a causal effect of ADHD genetic liability on subsequent major depression. However, findings were different for more broadly defined depression.

Polygenic risk for depression, anxiety and neuroticism are associated with the severity and rate of change in depressive symptoms across adolescence.

BACKGROUND: Adolescence marks a period where depression will commonly onset. Twin studies show that genetic influences play a role in how depression develops and changes across adolescence. Recent genome-wide association studies highlight that common genetic variants - which can be combined into polygenic risk scores (PRS) - are also implicated in depression. However, the role of PRS in adolescent depression and changes in adolescent depression is not yet understood. We aimed to examine associations between PRS for five psychiatric traits and depressive symptoms measured across adolescence using cross-sectional and growth-curve models. The five PRS were as follows: depression (DEP), major depressive disorder (MDD), anxiety (ANX), neuroticism (NEU) and schizophrenia (SCZ). METHODS: We used data from over 6,000 participants of the Avon Longitudinal Study of Parents and Children (ALSPAC) to examine associations between the five PRS and self-reported depressive symptoms (Short Mood and Feelings Questionnaire) over 9 occasions from 10 to 24 years. The PRS were created from well-powered genome-wide association studies conducted in adult populations. We examined cross-sectional associations between the PRS at each age and then again with longitudinal trajectories of depressive symptoms in a repeated measures framework using multilevel growth-curve analysis to examine the severity and the rate of change. RESULTS: There was strong evidence that higher PRS for DEP, MDD and NEU were associated with worse depressive symptoms throughout adolescence and into young adulthood in our cross-sectional analysis, with consistent associations observed across all nine occasions. Growth-curve analyses provided stronger associations (as measured by effect sizes) and additional insights, demonstrating that individuals with higher PRS for DEP, MDD and NEU had steeper trajectories of depressive symptoms across development, all with a greater increasing rate of change during adolescence. Evidence was less consistent for the ANX and SCZ PRS in the cross-sectional analysis, yet there was some evidence for an increasing rate of change in adolescence in the growth-curve analyses with the ANX PRS. CONCLUSIONS: These results show that common genetic variants as indexed by varying psychiatric PRS show patterns of specificity that influence both the severity and rate of change in depressive symptoms throughout adolescence and then into young adulthood. Longitudinal data that make use of repeated measures designs have the potential to provide greater insights how genetic factors influence the onset and persistence of adolescent depression.

Adverse childhood experiences and adult mood problems: evidence from a five-decade prospective birth cohort.

BACKGROUND: Retrospectively recalled adverse childhood experiences (ACEs) are associated with adult mood problems, but evidence from prospective population cohorts is limited. The aims of this study were to test links between prospectively ascertained ACEs and adult mood problems up to age 50, to examine the role of child mental health in accounting for observed associations, and to test gender differences in associations. METHODS: The National Child Development Study is a UK population cohort of children born in 1958. ACEs were defined using parent or teacher reports of family adversity (parental separation, child taken into care, parental neglect, family mental health service use, alcoholism and criminality) at ages 7-16. Children with no known (n = 9168), single (n = 2488) and multiple (n = 897) ACEs were identified in childhood. Adult mood problems were assessed using the Malaise inventory at ages 23, 33, 42 and 50 years. Associations were examined separately for males and females. RESULTS: Experiencing single or multiple ACEs was associated with increased rates of adult mood problems after adjustment for childhood psychopathology and confounders at birth [2+ v. 0 ACEs - men: age 23: odds ratio (OR) 2.36 (95% confidence interval (CI) 1.7-3.3); age 33: OR 2.40 (1.7-3.4); age 42: OR 1.85 (1.4-2.4); age 50: OR 2.63 (2.0-3.5); women: age 23: OR 2.00 (95% CI 1.5-2.6); age 33: OR 1.81 (1.3-2.5); age 42: OR 1.59 (1.2-2.1); age 50: OR 1.32 (1.0-1.7)]. CONCLUSIONS: Children exposed to ACEs are at elevated risk for adult mood problems and a priority for early prevention irrespective of the presence of psychopathology in childhood.

Practitioner review: Co-design of digital mental health technologies with children and young people.

BACKGROUND: There is increasing interest in digital technologies to help improve children and young people's mental health, and the evidence for the effectiveness for these approaches is rising. However, there is concern regarding levels of user engagement, uptake and adherence. Key guidance regarding digital health interventions stress the importance of early user input in the development, evaluation and implementation of technologies to help ensure they are engaging, feasible, acceptable and potentially effective. Co-design is a process of active involvement of stakeholders, requiring a change from the traditional approaches to intervention development. However, there is a lack of literature to inform the co-design of digital technologies to help child and adolescent mental health. METHODS: We reviewed the literature and practice in the co-design of digital mental health technologies with children and young people. We searched Medline, PsycInfo and Web of Science databases, guidelines, reviews and reference lists, contacted key authors for relevant studies, and extracted key themes on aspects of co-design relevant to practice. We supplemented this with case studies and methods reported by researchers working in the field. RESULTS: We identified 25 original articles and 30 digital mental health technologies that were designed/developed with children and young people. The themes identified were as follows: principles of co-design (including potential stakeholders and stages of involvement), methods of involving and engaging the range of users, co-designing the prototype and the challenges of co-design. CONCLUSIONS: Co-design involves all relevant stakeholders throughout the life and research cycle of the programme. This review helps to inform practitioners and researchers interested in the development of digital health technologies for children and young people. Future work in this field will need to consider the changing face of technology, methods of engaging with the diversity in the user group, and the evaluation of the co-design process and its impact on the technology.

Neuroendocrine and immune markers of maternal stress during pregnancy and infant cognitive development.

Antenatal exposure to maternal stress is a factor that may impact on offspring cognitive development. While some evidence exists of an association between maternal antenatal depressive or anxiety symptoms and infants' cognitive outcomes, less is known about the role of biological indices of maternal antenatal stress in relation to infant cognitive development. The current study investigated the association between maternal depressive and anxiety symptoms, stress and inflammatory markers during pregnancy and infant's cognitive development in a sample of 104 healthy pregnant women (mean gestational age = 34.76; SD = 1.12) and their 12-week-old infants (mean postnatal weeks = 11.96; SD = 1.85). Maternal depressive and anxiety symptoms were evaluated during pregnancy, alongside measurements of serum Interleukin-6 (IL-6), C-Reactive Protein (CRP), salivary cortisol, and alpha amylase (sAA) concentrations. Infant cognitive development, maternal caregiving and concurrent anxiety or depressive symptoms were assessed 12 weeks after delivery. Hierarchical linear regressions indicated that higher maternal diurnal cortisol and CRP levels were independently associated with lower infant cognitive development scores, while adjusting for infant gender and gestational age, maternal IQ, caregiving, depressive, or anxiety symptoms. Though correlational, findings seem suggestive of a role for variation in maternal biological stress signals during pregnancy in influencing infants' early cognitive development.

What explains the link between childhood ADHD and adolescent depression? Investigating the role of peer relationships and academic attainment.

There is increasing evidence that childhood Attention-Deficit Hyperactivity Disorder (ADHD) elevates risk of later depression, but the mechanisms behind this association are unclear. We investigated the relationship between childhood ADHD symptoms and late-adolescent depressive symptoms in a population cohort, and examined whether academic attainment and peer problems mediated this association. ALSPAC (Avon Longitudinal Study of Parents and Children) is an ongoing prospective longitudinal population-based UK cohort that has collected data since September 1990. 2950 individuals with data on parent-reported ADHD symptoms in childhood (7.5 years) and self-reported depressive symptoms in late adolescence (17.5 years) were included in analyses. 2161 individuals with additional data at age 16 years on parent-reported peer problems as an indicator of peer relationships and formal examination results (General Certificate of Secondary Education; GCSE) as an indicator of academic attainment were included in mediation analyses. Childhood ADHD symptoms were associated with higher depressive symptoms (b = 0.49, SE = 0.11, p < 0.001) and an increased odds of clinically significant depressive symptoms in adolescence (OR = 1.27, 95% CI 1.15-1.41, p < 0.001). The association with depressive symptoms was mediated in part by peer problems and academic attainment which accounted for 14.68% and 20.13% of the total effect, respectively. Childhood ADHD is associated with increased risk of later depression. The relationship is mediated in part by peer relationships and academic attainment. This highlights peer relationships and academic attainment as potential targets of depression prevention and intervention in those with ADHD. Future research should investigate which aspects of peer relationships are important in conferring later risk for depression.

Examining the relationship between stressful life events and overgeneral autobiographical memory in adolescents at high familial risk of depression.

Difficulty remembering specific events from the personal past, known as overgeneral autobiographical memory (AM), may be a marker of vulnerability to adolescent depression but little is known about how overgeneral AM arises in this age group. Stressful life events (SLEs) are strongly implicated in the onset of depression and are considered important in theoretical work on AM. We investigated whether exposure to lifetime and recent SLEs contributed to the development of overgeneral AM in a sample of adolescents at high familial risk of depression (n = 257) and examined the effects of gender and memory valence. Whether AM mediated the relationship between SLEs and MDD was also assessed. Exposure to a higher number of lifetime SLEs was associated with an increase in specific AMs. Associations of recent SLEs with AM differed by gender. For girls, more recent SLEs were associated with more overgeneral AMs. For boys, more recent SLEs were associated with fewer overgeneral AMs and more specific AMs. AM did not mediate the relationship between SLEs and subsequent DSM-IV depressive symptom count. Results suggest a complex relationship between AM and SLEs and that overgeneral AM and SLEs may have independent effects on future depression.

School achievement as a predictor of depression and self-harm in adolescence: linked education and health record study.

BACKGROUND: Mental disorders in children and adolescents have an impact on educational attainment. Aims To examine the temporal association between attainment in education and subsequent diagnosis of depression or self-harm in the teenage years. METHOD: General practitioner, hospital and education records of young people in Wales between 1999 and 2014 were linked and analysed using Cox regression. RESULTS: Linked records were available for 652 903 young people and of these 33 498 (5.1%) developed depression and 15 946 (2.4%) self-harmed after the age of 12 but before the age of 20. Young people who developed depression over the study period were more likely to have achieved key stage 1 (age 7 years) but not key stage 2 (age 11) (hazard ratio (HR) = 0.79, 95% CI 0.74-0.84) milestones, indicating that they were declining in academic attainment during primary school. Conversely, those who self-harmed were achieving as well as those who did not self-harm in primary school, but showed a severe decline in their attainment during secondary school (HR = 0.72, 95% CI 0.68-0.78). CONCLUSIONS: Long-term declining educational attainment in primary and secondary school was associated with development of depression in the teenage years. Self-harm was associated with declining educational attainment during secondary school only. Incorporating information on academic decline with other known risk factors for depression/self-harm (for example stressful life events, parental mental health problems) may improve risk profiling methods. Declaration of interest None.

The impact of schizophrenia and mood disorder risk alleles on emotional problems: investigating change from childhood to middle age.

BACKGROUND: Previous studies find that both schizophrenia and mood disorder risk alleles contribute to adult depression and anxiety. Emotional problems (depression or anxiety) begin in childhood and show strong continuities into adult life; this suggests that symptoms are the manifestation of the same underlying liability across different ages. However, other findings suggest that there are developmental differences in the etiology of emotional problems at different ages. To our knowledge, no study has prospectively examined the impact of psychiatric risk alleles on emotional problems at different ages in the same individuals. METHODS: Data were analyzed using regression-based analyses in a prospective, population-based UK cohort (the National Child Development Study). Schizophrenia and major depressive disorder (MDD) polygenic risk scores (PRS) were derived from published Psychiatric Genomics Consortium genome-wide association studies. Emotional problems were assessed prospectively at six time points from age 7 to 42 years. RESULTS: Schizophrenia PRS were associated with emotional problems from childhood [age 7, OR 1.09 (1.03-1.15), p = 0.003] to mid-life [age 42, OR 1.10 (1.05-1.17), p < 0.001], while MDD PRS were associated with emotional problems only in adulthood [age 42, OR 1.06 (1.00-1.11), p = 0.034; age 7, OR 1.03 (0.98-1.09), p = 0.228]. CONCLUSIONS: Our prospective investigation suggests that early (childhood) emotional problems in the general population share genetic risk with schizophrenia, while later (adult) emotional problems also share genetic risk with MDD. The results suggest that the genetic architecture of depression/anxiety is not static across development.

Identifying the contribution of prenatal risk factors to offspring development and psychopathology: What designs to use and a critique of literature on maternal smoking and stress in pregnancy.

Identifying prenatal environmental factors that have genuinely causal effects on psychopathology is an important research priority, but it is crucial to select an appropriate research design. In this review we explain why and what sorts of designs are preferable and focus on genetically informed/sensitive designs. In the field of developmental psychopathology, causal inferences about prenatal risks have not always been based on evidence generated from appropriate designs. We focus on reported links between maternal smoking during pregnancy and offspring attention-deficit/hyperactivity disorder or conduct problems. Undertaking a systematic review of findings from genetically informed designs and "triangulating" evidence from studies with different patterns of bias, we conclude that at present findings suggest it is unlikely that there is a substantial causal effect of maternal smoking in pregnancy on either attention-deficit/hyperactivity disorder or conduct problems. In contrast, for offspring birth weight (which serves as a positive control) findings strongly support a negative causal effect of maternal smoking in pregnancy. For maternal pregnancy stress, too few studies use genetically sensitive designs to draw firm conclusions, but continuity with postnatal stress seems important. We highlight the importance of moving beyond observational designs, for systematic evaluation of the breadth of available evidence and choosing innovative designs. We conclude that a broader set of prenatal risk factors should be examined, including those relevant in low- and middle-income contexts. Future directions include a greater use of molecular genetically informed designs such as Mendelian randomization to test causal hypotheses about prenatal exposure and offspring outcome.

Maternal depressive symptoms and adolescent academic attainment: Testing pathways via parenting and self-control.

Maternal depression is associated with reduced academic attainment in children, however, it is not clear how this association comes about. Depressive symptoms are associated with impairment in social roles including parenting. Children's self-control is an important contributor to academic attainment and is influenced by parenting. We therefore hypothesised that impaired parenting and children's self-control may mediate links between maternal depression and children's academic attainment. Data were from a brief longitudinal study (3 waves) of UK children aged 11-12 years and their mothers. Higher maternal depressive symptoms at baseline were associated with lower academic attainment in children assessed one year later. There was evidence to support an indirect effect of maternal depressive symptoms on children's academic attainment through the mother-child and the father-child relationship which, in turn, reduced children's self-control. These influences were independent of socio-economic deprivation. A direct effect of maternal depression on children's academic attainment was also observed.

The presentation of depression symptoms in attention-deficit/hyperactivity disorder: comparing child and parent reports.

BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) frequently co-occurs with depression, and outcomes are poor when both are present. Little is known about whether depression symptoms present differently in ADHD compared to the general population, or how reliable young people with ADHD are at reporting these symptoms. This study aimed to describe depression symptoms in a clinical ADHD sample compared to a population sample, and compare self-reports of depression symptoms with parent-reports. METHODS: Two hundred and forty-nine children with ADHD and their parents completed follow-up questionnaires around 5 years after taking part in a Cardiff University ADHD study. Child depression symptoms were measured using parent- and child-reported Mood and Feelings Questionnaires (MFQ) and compared to a population sample with MFQ data (n = 1460). Within both samples, child- and parent-reported depression symptoms were compared. RESULTS: Although the profile of depression symptoms was similar between young people with ADHD and those in the general population, depression symptoms were much more common in the ADHD sample (parent-rated MFQ score = 24.52 vs. 9.39; child-rated = 21.02 vs. 11.86). The most common symptoms in both samples included irritability, restlessness and concentration difficulties, with core depression symptoms such as feeling miserable/unhappy also prominent. Within the ADHD sample, but not the population sample, children reported depression symptoms less frequently than their parents. CONCLUSIONS: Young people with ADHD are at high risk of experiencing symptoms of depression but may under-report the severity of their symptoms. Obtaining parent reports of depression symptoms in this group may be important to avoid missing key indicators of risk.

Profiling depression in childhood and adolescence: the role of conduct problems.

BACKGROUND: Depression is typically more common in females and rates rise around puberty. However, studies of children and adolescents suggest that depression accompanied by conduct problems may represent a different subtype not characterised by a female preponderance, with differing risk factors and genetic architecture compared to pure-depression. This study aimed to identify aetiologically distinct profiles of depressive symptoms, distinguished by the presence or absence of co-occurring conduct problems. METHODS: Latent profile analysis was conducted on a school sample of 1648 children (11-12 years) and replicated in a sample of 2006 twins (8-17 years). RESULTS: In both samples pure-depressive and conduct-depressive profiles were identified. The pure-depressive profile was associated with female gender, while the conduct-depressive profile was associated with lower cognitive ability but not with gender. Twin analyses indicated possible differences in genetic aetiology. CONCLUSIONS: There was evidence for aetiologically heterogeneous depression symptom profiles based on the presence or absence of co-occurring conduct problems.

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.

A longitudinal study of self-control at the transition to secondary school: Considering the role of pubertal status and parenting.

Higher self-control in children and adolescents is associated with a range of positive outcomes in adulthood. However, little is known about the naturalistic development of self-control during early adolescence and the factors that affect this. We examined the role of puberty and parenting style as theoretically important influences on stability and change in self-control. A longitudinal (3 waves), multiple-informant dataset of children entering early adolescence (M = 11 years) was used to explore longitudinal change in self-control using latent growth curve modelling. Children's self-control declined during the one-year study period and declines were associated with children's behavioural and social functioning. Associations with self-control were found for pubertal status and parental warmth and hostility, but not for parental discipline. The findings suggest that during early adolescence, when children make the transition to secondary school, self-control declines. This is particularly the case for those experiencing puberty earlier than their peers. Parent warmth influences the trajectory of self-control during this period.

A longitudinal high-risk study of adolescent anxiety, depression and parent-severity on the developmental course of risk-adjustment.

BACKGROUND: Adolescence is associated with developments in the reward system and increased rates of emotional disorders. Familial risk for depression may be associated with disruptions in the reward system. However, it is unclear how symptoms of depression and anxiety influence the development of reward-processing over adolescence and whether variation in the severity of parental depression is associated with hyposensitivity to reward in a high-risk sample. METHODS: We focused on risk-adjustment (adjusting decisions about reward according to the probability of obtaining reward) as this was hypothesized to improve over adolescence. In a one-year longitudinal sample (N = 197) of adolescent offspring of depressed parents, we examined how symptoms of depression and anxiety (generalized anxiety and social anxiety) influenced the development of risk-adjustment. We also examined how parental depression severity influenced adolescent risk-adjustment. RESULTS: Risk-adjustment improved over the course of the study indicating improved adjustment of reward-seeking to shifting contingencies. Depressive symptoms were associated with decreases in risk-adjustment over time while social anxiety symptoms were associated with increases in risk-adjustment over time. Specifically, depression was associated with reductions in reward-seeking at favourable reward probabilities only, whereas social anxiety (but not generalized anxiety) led to reductions in reward-seeking at low reward probabilities only. Parent depression severity was associated with lowered risk-adjustment in offspring and also influenced the longitudinal relationship between risk-adjustment and offspring depression. CONCLUSIONS: Anxiety and depression distinctly alter the pattern of longitudinal change in reward-processing. Severity of parent depression was associated with alterations in adolescent offspring reward-processing in a high-risk sample.