The Mood and Resilience in Offspring (MARIO) project: a longitudinal cohort study among offspring of parents with and without a mood disorder.

BACKGROUND: One of the most robust risk factors for developing a mood disorder is having a parent with a mood disorder. Unfortunately, mechanisms explaining the transmission of mood disorders from one generation to the next remain largely elusive. Since timely intervention is associated with a better outcome and prognosis, early detection of intergenerational transmission of mood disorders is of paramount importance. Here, we describe the design of the Mood and Resilience in Offspring (MARIO) cohort study in which we investigate: 1. differences in clinical, biological and environmental (e.g., psychosocial factors, substance use or stressful life events) risk and resilience factors in children of parents with and without mood disorders, and 2. mechanisms of intergenerational transmission of mood disorders via clinical, biological and environmental risk and resilience factors. METHODS: MARIO is an observational, longitudinal cohort study that aims to include 450 offspring of parents with a mood disorder (uni- or bipolar mood disorders) and 100-150 offspring of parents without a mood disorder aged 10-25 years. Power analyses indicate that this sample size is sufficient to detect small to medium sized effects. Offspring are recruited via existing Dutch studies involving patients with a mood disorder and healthy controls, for which detailed clinical, environmental and biological data of the index-parent (i.e., the initially identified parent with or without a mood disorder) is available. Over a period of three years, four assessments will take place, in which extensive clinical, biological and environmental data and data on risk and resilience are collected through e.g., blood sampling, face-to-face interviews, online questionnaires, actigraphy and Experience Sampling Method assessment. For co-parents, information on demographics, mental disorder status and a DNA-sample are collected. DISCUSSION: The MARIO cohort study is a large longitudinal cohort study among offspring of parents with and without mood disorders. A unique aspect is the collection of granular data on clinical, biological and environmental risk and resilience factors in offspring, in addition to available parental data on many similar factors. We aim to investigate the mechanisms underlying intergenerational transmission of mood disorders, which will ultimately lead to better outcomes for offspring at high familial risk.

A theory-informed emotion regulation variability index: Bray-Curtis dissimilarity.

Emotion regulation (ER) variability refers to how individuals vary their use of ER strategies across time. It helps individuals to meet contextual needs, underscoring its importance in well-being. The theoretical foundation of ER variability recognizes two constituent processes: strategy switching (e.g., moving from distraction to social sharing) and endorsement change (e.g., decreasing the intensity of both distraction and social sharing). ER variability is commonly operationalized as the SD between strategies per observation (between-strategy SD) or within a strategy across time (within-strategy SD). In this article, we show that these SD-based approaches cannot sufficiently capture strategy switching and endorsement change, leading to ER variability indices with poor validity. We propose Bray-Curtis dissimilarity, a measure used in ecology to quantify biodiversity variability, as a theory-informed ER variability index. First, we demonstrate how Bray-Curtis dissimilarity is more sensitive than SD-based approaches in detecting ER variability through two simulation studies. Second, assuming that higher ER variability is adaptive in daily life, we test the relation between ER variability and negative affect in three experience sampling method data sets (total N = [70, 95, 200], number of moment-level observations = [5,040, 6,329, 14,098]). At both the moment level and person level, higher Bray-Curtis dissimilarity predicted lower negative affect more consistently than SD-based indices. We conclude that Bray-Curtis dissimilarity may better capture moment-level within-person ER variability and could have implications for studying variability in other multivariate dynamic processes. The article is accompanied by an R tutorial and practical recommendations for using Bray-Curtis dissimilarity with experience sampling method data. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Risk-related brain activation is linked to longitudinal changes in adolescent health risk behaviors.

Middle adolescence is the period of development during which youth begin to engage in health risk behaviors such as delinquent behavior and substance use. A promising mechanism for guiding adolescents away from risky choices is the extent to which adolescents are sensitive to the likelihood of receiving valued outcomes. Few studies have examined longitudinal change in adolescent risky decision making and its neural correlates. To this end, the present longitudinal three-wave study (Nw1 = 157, Mw1= 13.50 years; Nw2 = 148, Mw2= 14.52 years; Nw3 = 143, Mw3= 15.55 years) investigated the ontogeny of mid-adolescent behavioral and neural risk sensitivity, and their baseline relations to longitudinal self-reported health risk behaviors. Results showed that adolescents became more sensitive to risk both in behavior and the brain during middle adolescence. Across three years, we observed lower risk-taking and greater risk-related activation in the bilateral insular cortex. When examining how baseline levels of risk sensitivity were related to longitudinal changes in real-life health risk behaviors, we found that Wave 1 insular activity was related to increases in self-reported health risk behaviors over the three years. This research highlights the normative maturation of risk-related processes at the behavioral and neural levels during mid-adolescence.

Weighing poor immunometabolic health in relatives for severity of affective symptoms: A study of patients with depressive and anxiety disorders and their siblings.

BACKGROUND: Affective (i.e. depressive and anxiety) disorders often co-occur with immunometabolic diseases and related biological pathways. Although many large population-based and meta-analytic studies have confirmed this link in community and clinical samples, studies in at-risk samples of siblings of persons with affective disorders are lacking. Furthermore, this somatic-mental co-occurrence may be partially explained by familial clustering of the conditions. First, we examined whether the association between a wide range of immunometabolic diseases and related biomarker based risk-profiles with psychological symptoms replicates in at-risk siblings of probands with affective disorders. Second, leveraging on a sibling-pair design, we disentangled and quantified the effect of probands' immunometabolic health on siblings' psychological symptoms and on the association between immunometabolic health and these symptoms in siblings. METHODS: The sample included 636 participants (Mage = 49.7; 62.4% female) from 256 families, each including a proband with lifetime depressive and/or anxiety disorders and at least one of their sibling(s) (N = 380 proband-sibling pairs). Immunometabolic health included cardiometabolic and inflammatory diseases, body mass index (BMI), and composite metabolic (based on the five metabolic syndrome components) and inflammatory (based on interleukin-6 and C-reactive protein) biomarker indices. Overall affective symptoms and specific atypical, energy-related depressive symptoms were derived from self-report questionnaires. Mixed-effects analyses were used to model familial clustering. RESULTS: In siblings, inflammatory disease (γ = 0.25, p = 0.013), higher BMI (γ = 0.10, p = 0.033) and metabolic index (γ = 0.28, p < 0.001) were associated with higher affective symptoms, with stronger associations for atypical, energy-related depressive symptoms (additionally associated with cardiometabolic disease; γ = 0.56, p = 0.048). Immunometabolic health in probands was not independently associated with psychological symptoms in siblings nor did it moderate the association between immunometabolic health and psychological symptoms estimated in siblings. CONCLUSIONS: Our findings demonstrate that the link between later life immunometabolic health and psychological symptoms is consistently present also in adult siblings at high risk for affective disorders. Familial clustering did not appear to have a substantial impact on this association. Instead, individual lifestyle, rather than familial factors, may have a relatively higher impact in the clustering of later life immunometabolic conditions with psychological symptoms in at-risk adult individuals. Furthermore, results highlighted the importance of focusing on specific depression profiles when investigating the overlap with immunometabolic health.

Interplay between genetic risk and the parent environment in adolescence and substance use in young adulthood: A TRAILS study.

Many adolescents start using tobacco, alcohol, and cannabis. Genetic vulnerability, parent characteristics in young adolescence, and interaction (GxE) and correlation (rGE) between these factors could contribute to the development of substance use. Using prospective data from the TRacking Adolescent Individuals' Lives Survey (TRAILS; N = 1,645), we model latent parent characteristics in young adolescence to predict young adult substance use. Polygenic scores (PGS) are created based on genome-wide association studies (GWAS) for smoking, alcohol use, and cannabis use. Using structural equation modeling we model the direct, GxE, and rGE effects of parent factors and PGS on young adult smoking, alcohol use, and cannabis initiation. The PGS, parental involvement, parental substance use, and parent-child relationship quality predicted smoking. There was GxE such that the PGS amplified the effect of parental substance use on smoking. There was rGE between all parent factors and the smoking PGS. Alcohol use was not predicted by genetic or parent factors, nor by interplay. Cannabis initiation was predicted by the PGS and parental substance use, but there was no GxE or rGE. Genetic risk and parent factors are important predictors of substance use and show GxE and rGE in smoking. These findings can act as a starting point for identifying people at risk.

Weighing psychosocial factors in relatives for the risk of psychopathology: a study of patients with depressive and anxiety disorders and their siblings.

PURPOSE: Siblings of probands with depressive and anxiety disorders are at increased risk for psychopathology, but little is known about how risk factors operate within families to increase psychopathology for siblings. We examined the additional impact of psychosocial risk factors in probands-on top of or in combination with those in siblings-on depressive/anxious psychopathology in siblings. METHODS: The sample included 636 participants (Mage = 49.7; 62.4% female) from 256 families, each including a proband with lifetime depressive and/or anxiety disorders and their sibling(s) (N = 380 proband-sibling pairs). Sixteen psychosocial risk factors were tested. In siblings, depressive and anxiety disorders were determined with standardized psychiatric interviews; symptom severity was measured using self-report questionnaires. Analyses were performed with mixed-effects models accounting for familial structure. RESULTS: In siblings, various psychosocial risk factors (female gender, low income, childhood trauma, poor parental bonding, being single, smoking, hazardous alcohol use) were associated with higher symptomatology and likelihood of disorder. The presence of the same risk factor in probands was independently associated (low income, being single) with higher symptomatology in siblings or moderated (low education, childhood trauma, hazardous alcohol use)-by reducing its strength-the association between the risk factor and symptomatology in siblings. There was no additional impact of risk factors in probands on likelihood of disorder in siblings. CONCLUSION: Our findings demonstrate the importance of weighing psychosocial risk factors within a family context, as it may provide relevant information on the risk of affective psychopathology for individuals.

Behavioral inhibition, negative parenting, and social withdrawal: Longitudinal associations with loneliness during early, middle, and late adolescence.

Adolescent loneliness can have detrimental effects on physical and mental health, but there is limited understanding of its antecedents in infancy and childhood. A 20-year longitudinal, multi-informant, and multi-methods study (first data collection in 1998) was conducted to examine mechanisms underlying adolescent loneliness (N = 128, 52% boys, Mage_baseline  = 1.23, SD = 0.02, 99% White, recruitment in Dutch urban, healthcare centers). Structural equation modeling showed that high infant behavioral inhibition (BI) was indirectly associated with high loneliness during adolescence via high childhood social withdrawal. This indirect effect was equally strong during early, middle, and late adolescence. Contrary to expectations, infant parenting did not moderate the relation between BI and social withdrawal. The results suggest a developmental cascade with infant BI showing long-lasting indirect effects on adolescent loneliness up to 20 years later via childhood social withdrawal.

Prosocial Behavior and Aggression in the Daily School Lives of Early Adolescents.

Research has not adequately addressed a possible mutual co-regulatory influence of prosocial and aggressive behaviors in adolescents' daily lives. This study explored bidirectional within-person associations between prosocial and aggressive behaviors in the daily school lives of early adolescents. The sample included 242 sixth-graders [Mage = 11.96 (SD = 0.18), 50% girls] and their teachers. Adolescents reported on daily prosocial behavior and reactive and proactive aggression for ten consecutive days. Teachers and adolescents reported on adolescents' overall prosocial behaviors. Across-day prosocial behaviors increased after days when adolescents exhibited more reactive aggression but not among self-reported low-prosocial adolescents. Increased prosocial behaviors did not mitigate aggression the next day. The findings suggest prosocial behaviors are a plausible compensatory strategy after daily aggressive reactions.

[Prevention of psychopathology in children: Interventions for intergenerational transmission]. / Preventie psychologische stoornissen bij kinderen.

Children of parents with anxiety or mood disorders have an increased risk of developing an anxiety or mood disorder themselves. A qualitative review of different components of well-studied prevention programs shows that all programs use elements of psychoeducation. Programs that primarily target children often use elements of cognitive behavioral therapy. Programs aimed at the whole family contain components focused on communication between family members and parenting skills. In general, these prevention programs are effective in preventing short- and long-term anxiety/mood disorders and reducing existing symptoms in children. Future research should pay more attention to how and for whom the prevention programs are effective. Primary health care plays an important role in identifying children at risk, underscoring the importance of training professionals in early signaling psychopathology in parents and children. Children with mild complaints could be identified earlier, possibly preventing more serious problems and intensive treatment processes.

Familial risk for depressive and anxiety disorders: associations with genetic, clinical, and psychosocial vulnerabilities.

BACKGROUND: In research and clinical practice, familial risk for depression and anxiety is often constructed as a simple Yes/No dichotomous family history (FH) indicator. However, this measure may not fully capture the liability to these conditions. This study investigated whether a continuous familial loading score (FLS), incorporating family- and disorder-specific characteristics (e.g. family size, prevalence of depression/anxiety), (i) is associated with a polygenic risk score (PRS) for major depression and with clinical/psychosocial vulnerabilities and (ii) still captures variation in clinical/psychosocial vulnerabilities after information on FH has been taken into account. METHODS: Data came from 1425 participants with lifetime depression and/or anxiety from the Netherlands Study of Depression and Anxiety. The Family Tree Inventory was used to determine FLS/FH indicators for depression and/or anxiety. RESULTS: Persons with higher FLS had higher PRS for major depression, more severe depression and anxiety symptoms, higher disease burden, younger age of onset, and more neuroticism, rumination, and childhood trauma. Among these variables, FH was not associated with PRS, severity of symptoms, and neuroticism. After regression out the effect of FH from the FLS, the resulting residualized measure of FLS was still associated with severity of symptoms of depression and anxiety, rumination, and childhood trauma. CONCLUSIONS: Familial risk for depression and anxiety deserves clinical attention due to its associated genetic vulnerability and more unfavorable disease profile, and seems to be better captured by a continuous score that incorporates family- and disorder-specific characteristics than by a dichotomous FH measure.

Familial resemblance in mental health symptoms, social and cognitive vulnerability, and personality: A study of patients with depressive and anxiety disorders and their siblings.

BACKGROUND: Investigating siblings of probands with affective disorders enables the identification of psychopathology-related risk features. Leveraging data from an older adult sample, as compared to most previous sibling studies, enabled us to study more definitive clinical profiling across the lifespan. We examined prevalence of depressive/anxiety disorders in siblings, proband-sibling resemblance in psychopathology-related features, and whether unaffected siblings showed higher levels of these features than healthy controls. METHODS: The sample (N=929; Mage=50.6) consisted of 256 probands with lifetime depressive and/or anxiety disorders, their 380 siblings, and 293 healthy controls without affected relatives. Fifteen psychopathology-related features were investigated across four domains: mental health symptoms, social vulnerabilities, cognitive vulnerabilities, and personality. RESULTS: Lifetime disorders were present in 50.3% of siblings. Prevalence was 2-3 times higher than Dutch population frequencies. We found small to medium probandsibling resemblance across psychopathology-related features (ρ=0.10-0.32). Unaffected siblings reported poorer interpersonal functioning and more negative life events, childhood trauma, and rumination than healthy controls. LIMITATIONS: Due to the cross-sectional study design, the directionality of effects cannot be determined. No inferences can be made about potential differences in familial resemblance in psychopathology-related features between high- and low-risk families. CONCLUSIONS: Siblings of probands with affective disorders are at higher risk for depressive/anxiety disorders. Even when unaffected, still show higher psychosocial vulnerability than healthy controls. Nevertheless, the only modest proband-sibling resemblance across psychopathology-related features suggests that individual mechanisms differentiate clinical trajectories across the lifespan. Identification of these mechanisms is crucial to improve resilience in subjects with familial risk.

Guideline concordance and outcome in long-term naturalistic treatment of bipolar disorder - a one-year longitudinal study using latent change models.

BACKGROUND: Only few studies investigated the relation between concordance with treatment guidelines and treatment outcome in everyday treatment of bipolar disorder (BD). Prospective studies are scarce. METHODS: A nationwide, naturalistic, prospective study on the relation between guideline concordance and treatment outcome in the long-term outpatient treatment of patients with BD. Participants completed a survey on treatments received and various outcome measures at baseline and after one year. RESULTS: Of 839 patients who completed the baseline survey, 615 (73.3%) also completed the follow-up survey. Consistent with our a priori hypothesis, cross-sectional analyses at baseline showed correlations between guideline concordance with quality of life (r = .17, p < .001), treatment satisfaction (r = .17, p <.001), and impaired functioning (r = -.10, p = .04). At follow-up, guideline concordance was correlated with severity of illness (r = -.10, p = .05), quality of life (r = .18, p < .001), and treatment satisfaction (r = .15, p < .001). Concerning three additional hypotheses on longitudinal relations between concordance and outcome measures, only a positive relation was found between change in guideline concordance and change in quality of life. LIMITATIONS: Selection bias may have occurred by inclusion of patients with neither a very severe nor a very mild course of illness. CONCLUSIONS: Although guideline concordance was high throughout the study, change in guideline concordance was positively associated with change in quality of life, suggesting that especially in long-term treatment, continuous efforts to optimize ongoing treatment is essential.

Human responses to Covid-19: The role of optimism bias, perceived severity, and anxiety.

During the Covid-19 pandemic, the governments are trying to contain the spread with non-pharmaceutical interventions (NPIs), such as social distancing rules, restrictions, and lockdowns. In an effort to identify factors that may influence population adherence to NPIs, we examined the role of optimism bias, anxiety, and perceived severity of the situation in relation to engagement in protective behavioral changes and satisfaction with governments' response to this pandemic. We conducted an online survey in 935 participants (M age  = 34.29; 68.88% females) that was disseminated in April and May 2020 in the Netherlands, Germany, Greece, and USA. Individuals with high optimism bias engaged less in behavioral changes, whereas individuals with high levels of anxiety and high perceived severity engaged more in behavioral changes. Individuals with high optimism bias and high levels of anxiety were less satisfied with the governments' response, albeit for different reasons. Individuals who reported low perceived severity and low government satisfaction engaged the least in behavioral changes, whereas participants who reported high perceived severity and low government satisfaction engaged the most in behavioral changes. This study contributes to a better understanding of the psychological factors that influence people's responses to NPIs.

Grumpy or depressed? Disentangling typically developing adolescent mood from prodromal depression using experience sampling methods.

INTRODUCTION: This study aimed at differentiating normative developmental turmoil from prodromal depressive symptoms in adolescence. METHOD: Negative and positive mood (daily) in different contexts (friends, home, school), and (subsequent) depressive symptoms were assessed in Dutch adolescents. RESULTS & CONCLUSION: Mixture modeling on one cross-sectional study, using a newly developed questionnaire (CSEQ; subsample 1a; n = 571; girls 55.9%; Mage = 14.17) and two longitudinal datasets with Experience Sampling Methods data (subsample 1b: n = 241; Mage = 13.81; 62.2% girls, sample 2: n = 286; 59.7% girls; Mage = 14.19) revealed three mood profiles: 18-24% "happy", 43-53% "typically developing", and 27-38% "at-risk". Of the "at-risk" profile between 12.5% and 25% of the adolescents scored above the clinical cut-off for depression. These mood profiles predicted later depressive symptoms, while controlling for earlier symptoms. In subsample 1b, parents were not always aware of the mental health status of their adolescent.

Longitudinal associations between negative life events and depressive symptoms-A 9-year longitudinal study on between-person and within-person effects and the role of family history.

Research has shown that negative life events contribute to the development of depression. Moreover, it has been suggested that individuals with a family history of depression experience more negative life events and are more susceptible to the effect of negative life events. However, previous studies did not differentiate stable between-person effects (interindividual differences) and temporal within-person effects (intraindividual differences). This study aims to examine the bidirectional relation between negative life events and depressive symptoms using a novel statistical method (i.e., a random intercept cross-lagged panel model) that allows to separate within-person from between-person processes. Second, we examined the role of family history in that relation. Data came from 1,771 adults (1,320 with a depressive and/or anxiety disorder, 451 controls) that were followed over 9 years (baseline, 2-, 4-, 6-, and 9-year follow-up). Questionnaires were used to measure depressive symptoms and the number of independent (i.e., events independent of someone's symptoms) and dependent negative life events (i.e., events more likely to be influenced by a person). Results showed that individuals with more negative life events experienced more depressive symptoms on a between-person level. Additionally, although the effects were considerably smaller, results suggested within-person increases in dependent and independent negative life events were correlated with within-person increases in depressive symptoms. Overall, our results suggest that negative life events and depressive symptoms are more consistently associated on a between-person than on a within-person level. Thus, negative life events may rather explain differences in depressive symptoms between persons than within persons. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Prevention programmes for children of parents with a mood/anxiety disorder: Systematic review of existing programmes and meta-analysis of their efficacy.

OBJECTIVES: To systematically describe the characteristics and techniques of prevention programmes for children of parents with mood/anxiety disorders. In addition, recruitment approaches and difficulties were identified and a meta-analysis was conducted to examine the efficacy of these prevention programmes. METHODS: Randomized controlled trials assessing the efficacy of a prevention programme for children (6-25 years) of parents with mood and/or anxiety disorders were included. A systematic literature search was conducted in PubMed, PsychINFO, and CENTRAL from the earliest record to March 2019. In addition, programme manuals of identified prevention programmes were requested for a content analysis. RESULTS: Twenty-two articles containing eight unique prevention programmes involving 1,325 subjects were identified. Programmes varied in the number and types of techniques, but all provided psychoeducation. Results suggested that recruitment via clinicians was more successful than recruitment via health maintenance organization databases. In a meta-analysis, a significant risk difference was found in favour of prevention programmes on the risk of developing a depressive/anxiety disorder in offspring at short-term (9-18 months follow-up; RR = 0.37, 95% CI [0.21; 0.66]) and long-term follow-up (24 months or longer follow-up; RR = 0.71, 95% CI [0.57; 0.87] and on symptom levels in offspring at post-intervention (SMD = -0.19, 95% CI [-0.36; -0.02]) and at 12-months follow-up (SMD = -0.31, 95% CI [-0.57; -0.06]). CONCLUSIONS: The prevention programmes combined psychoeducational elements with skills training and/or cognitive-behavioural therapy elements. The recruitment process and the content of these programmes are sometimes insufficiently described. Nevertheless, they appear to be effective, indicating a need to further examine how these programmes exactly work and for whom. PRACTITIONER POINTS: Preventive interventions for children of parents with mood/anxiety disorders appear to be effective in preventing these disorders in offspring. Available preventive intervention programmes focus mostly on psychoeducation, cognitive-behavioural therapy, and family processes. More effort should be made into describing preventive interventions so that they can be easily implemented by practitioners. Studies should further examine why and for whom preventive interventions for children of parents with mood/anxiety disorders are effective.

It is a family affair: individual experiences and sibling exposure to emotional, physical and sexual abuse and the impact on adult depressive symptoms.

BACKGROUND: Childhood abuse and neglect often occurs within families and can have a large influence on mental well-being across the lifespan. However, the sibling concordance of emotional abuse and neglect (i.e. together referred to as emotional maltreatment; EM), physical abuse (PA) and sexual abuse (SA) and the long-term impact on the context of siblings' maltreatment experiences are unclear. To examine the influence of EM, PA and SA on adult depressive symptoms within the family framework we differentiate between (a) the family-wide (mean level of all siblings) effects and (b) the individual deviation from the mean family level of maltreatment. METHODS: The sample (N = 636) consists of 256 families, including at least one lifetime depressed or anxious individual and their siblings. Multilevel modeling was used to examine the family-wide and relative individual effects of childhood maltreatment (CM). RESULTS: (a) Siblings showed most similarity in their reports of EM followed by PA. SA was mostly reported by one person within a family. In line with these observations, the mean family levels of EM and PA, but not SA, were associated with more depressive symptoms. In addition, (b) depression levels were more elevated in individuals reporting more EM than the family mean. CONCLUSIONS: Particularly in the case of more visible forms of CM, siblings' experiences of EM and PA are associated with the elevated levels of adult depressive symptoms. Findings implicate that in addition to individual maltreatment experiences, the context of siblings' experiences is another crucial risk factor for an individuals' adult depressive symptomatology.

Genetic aetiology of self-harm ideation and behaviour.

Family studies have identified a heritable component to self-harm that is partially independent from comorbid psychiatric disorders. However, the genetic aetiology of broad sense (non-suicidal and suicidal) self-harm has not been characterised on the molecular level. In addition, controversy exists about the degree to which suicidal and non-suicidal self-harm share a common genetic aetiology. In the present study, we conduct genome-wide association studies (GWAS) on lifetime self-harm ideation and self-harm behaviour (i.e. any lifetime self-harm act regardless of suicidal intent) using data from the UK Biobank (n > 156,000). We also perform genome wide gene-based tests and characterize the SNP heritability and genetic correlations between these traits. Finally, we test whether polygenic risk scores (PRS) for self-harm ideation and self-harm behaviour predict suicide attempt, suicide thoughts and non-suicidal self-harm (NSSH) in an independent target sample of 8,703 Australian adults. Our GWAS results identified one genome-wide significant locus associated with each of the two phenotypes. SNP heritability (hsnp2) estimates were ~10%, and both traits were highly genetically correlated (LDSC rg > 0.8). Gene-based tests identified seven genes associated with self-harm ideation and four with self-harm behaviour. Furthermore, in the target sample, PRS for self-harm ideation were significantly associated with suicide thoughts and NSSH, and PRS for self-harm behaviour predicted suicide thoughts and suicide attempt. Follow up regressions identified a shared genetic aetiology between NSSH and suicide thoughts, and between suicide thoughts and suicide attempt. Evidence for shared genetic aetiology between NSSH and suicide attempt was not statistically significant.

Parental bonding: Psychometric properties and association with lifetime depression and anxiety disorders.

In epidemiology and psychiatry research, the Parental Bonding Instrument (PBI) is commonly used to assess offspring's perception on maternal and paternal behavior during childhood. We tested the 2- versus 3-factor structure of the 16-item version and assessed measurement invariance across sex and across lifetime depressed, anxious, comorbid affected, and healthy participants. Subsequently, we investigated PBI dimensions across sex and psychopathology groups using structural equation modeling. Participants were 2,069 adults with a lifetime affective disorder and healthy controls, ages 26-75, from the Netherlands. Our findings support the 3-factor solution of the distinct mother and father scales, distinguishing care, overprotection, and autonomy (previously "authoritarianism"). Moreover, measurement of the PBI appeared to be invariant across groups, indicating that means and relations can be reliably compared across sex and psychopathology groups. Men reported more maternal overprotection and paternal lack of care, whereas females reported higher paternal and maternal lack of autonomy and maternal lack of care levels compared with males. Lack of care and lack of autonomy levels were elevated in all affected groups, with the comorbid group showing highest levels of all 3 PBI dimensions. Adults with anxiety disorders reported heightened maternal lack of autonomy levels compared with the depression group and healthy controls. Adults with a depressive disorder reported heightened paternal lack of care levels as compared with the anxiety group and healthy controls. We advocate to use the 3-factor structure and conclude that suboptimal parental bonding, mainly lack of care and lack of autonomy, is associated with lifetime anxiety and depression. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Neural Cognitive Control Moderates the Relation between Negative Life Events and Depressive Symptoms in Adolescents.

The present longitudinal study examined the role of neural cognitive control in the relation between negative and positive life events and depressive symptoms in adolescents. The sample comprised 138 adolescents (52% male, Mage = 13.49 at baseline) and their parents. At Time 1, adolescents participated in a functional neuroimaging session in which neural cognitive control was measured as hemodynamic activity during an inhibitory control task, and parents reported on adolescents' positive and negative life events within the past year. Adolescents and parents reported on adolescent depressive symptoms at Time 1, Time 2 (1 year later), and Time 3 (2 years later). Conditional latent growth curve model was used to test the main and interaction effects of neural cognitive control and positive/negative life events on the growth factors of depressive symptoms. Higher neural cognitive control moderated the relation between negative life events and the intercept of depressive symptoms. Adolescents with higher neural cognitive control did not experience higher depressive symptoms when confronted with more negative life events, whereas their counterparts with lower neural cognitive control did. The interaction effect between neural cognitive control and positive life events on depressive symptoms was not significant. Results suggest that neural cognitive control acts as a protective factor such that adolescents with higher neural cognitive control are protected against depressionogenic effects of negative life events, whereas adolescents with lower cognitive control are at greater risk for depressive symptoms in response to negative life events.