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The Genesis 12-19 (G1219) Study is an ongoing longitudinal study of a sample of UK twin pairs, non-twin sibling pairs, and their parents. G1219 was initially designed to examine the role of gene-environment interplay in adolescent depression. However, since then data have continued to be collected from both parents and their offspring into young adulthood. This has allowed for longitudinal analyses of depression and has enabled researchers to investigate multiple phenotypes and to ask questions about intermediate mechanisms. The study has primarily focused on emotional development, particularly depression and anxiety, which have been assessed at multiple levels of analysis (symptoms, cognitions, and relevant environmental experiences). G1219 has also included assessment of a broader range of psychological phenotypes ranging from antisocial behaviors and substance use to sleep difficulties, in addition to multiple aspects of the environment. DNA has also been collected. The first wave of data collection began in the year 1999 and the fifth wave of data collection will be complete before the end of 2012. In this article, we describe the sample, data collection, and measures used. We also summarize some of the key findings to date. [ABSTRACT FROM AUTHOR]

Background: ADHD symptoms are associated with emotional problems such as depressive and anxiety symptoms from early childhood to adulthood, with the association increasing with age. A shared aetiology and/or a causal relationship could explain their correlation. In the current study, we explore these explanations for the association between ADHD symptoms and emotional problems from childhood to adulthood., Methods: Data were drawn from the Twins Early Development Study (TEDS), including 3675 identical and 7063 non-identical twin pairs. ADHD symptoms and emotional symptoms were reported by parents from childhood to adulthood. Self-report scales were included from early adolescence. Five direction of causation (DoC) twin models were fitted to distinguish whether associations were better explained by shared aetiology and/or causal relationships in early childhood, mid-childhood, early adolescence, late adolescence, and early adulthood. Follow-up analyses explored associations for the two subdomains of ADHD symptoms, hyperactivity-impulsivity and inattention, separately., Results: The association between ADHD symptoms and emotional problems increased in magnitude from early childhood to adulthood. In the best-fitting models, positive genetic overlap played an important role in this association at all stages. A negative causal effect running from ADHD symptoms to emotional problems was also detected in early childhood and mid-childhood. When distinguishing ADHD subdomains, the apparent protective effect of ADHD symptoms on emotional problems in childhood was mostly driven by hyperactivity-impulsivity., Conclusions: Genetic overlap plays an important role in the association between ADHD symptoms and emotional problems. Hyperactivity-impulsivity may protect children from emotional problems in childhood, but this protective effect diminishes after adolescence.

Background: Experiences of racism are linked to negative physical and mental health outcomes among those exposed. According to quantitative research derived mainly from the United States, these negative outcomes can have cascading effects in families, when parents' experiences of racism indirectly impact offspring. New research is warranted for families in the United Kingdom, informed by a qualitative approach to canvassing community knowledge and perspectives, exploring how existing findings relate to lived experiences., Method: We conducted four online focus groups with 14 parents of school-aged children and 14 adolescents who had experienced racism in the United Kingdom. Participants were asked what children know of parents' experiences of racism, and how these experiences can impact parent-child interactions, mental health and well-being. Focus group recordings were transcribed, data coded and analysed through iterative categorisation., Results: Analyses drew four themes from participants' insights. Together, themes illuminated the pervasive nature of racism experienced by some families in the United Kingdom. Parent and child experiences of racism were connected and co-occurring, with indirect effects impacting mental health and well-being in both generations. These experiences were linked to both positive and negative changes in parenting behaviour and parent-child relationships, which could be moderated by intersecting identities such as the parent's generational status for immigration to the United Kingdom. Social cohesion, safe spaces and education programmes were highlighted for future intervention., Conclusions: Findings corroborate existing literature, while further emphasising a broader bidirectional picture, requiring a family system and intersectional approach to understanding the mental health impact of racism in families. Avenues for future research are discussed to support development of equitable intervention and support strategies to prevent racism and support those affected., (© 2024 The Authors. Child and Adolescent Mental Health published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

The United States is a nation of diverse racial and ethnic origins. Athletes represent the full spectrum of the nation's population. However, the orthopedic surgeons who serve as team physicians are Caucasian and male with staggeringly few exceptions. This manuscript provides an overview of the current status and barriers to diversity among orthopedic team physicians, along with strategies to address the issue. Specifically, pipeline initiatives implemented at one academic medical school and orthopedic surgery department are summarized as potential models that can be further developed by other institutions to enhance diversity in orthopedic surgery., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Low socioeconomic status (SES) is associated with increased risk for emotional and behavioural problems among children. Evidence from twin studies has shown that family SES moderates genetic and environmental influences on child mental health. However, it is also known that SES is itself under genetic influence and previous gene-environment interaction (G×E) studies have not incorporated the potential genetic overlap between child mental health and family SES into G×E analyses. We applied a novel approach using extended family data to investigate the moderation of aetiological influences on child emotional and behavioural problems by parental socioeconomic status in the presence of modelled gene-environment correlation., Methods: The sample comprised >28,100 children in extended-family units drawn from the Norwegian Mother, Father and Child Cohort Study (MoBa). Mothers reported children's emotional and behavioural symptoms. Parents' income and educational attainment were obtained through linkage to administrative register data. Bivariate moderation Multiple-Children-of-Twins-and-Siblings (MCoTS) models were used to analyse relationships between offspring outcomes (emotional and behavioural symptom scores) and parental socioeconomic moderators (income rank and educational attainment)., Results: The aetiology of child emotional symptoms was moderated by maternal and paternal educational attainment. Shared environmental influences on child emotional symptoms were greater at lower levels of parents' education. The aetiology of child behavioural symptoms was moderated by maternal, but not paternal, socioeconomic factors. Genetic factors shared between maternal income and child behavioural symptoms were greater in families with lower levels maternal income. Nonshared environmental influences on child behavioural symptoms were greater in families with higher maternal income and education., Conclusions: Parental socioeconomic indicators moderated familial influences and nonshared environmental influences on child emotional and behavioural outcomes. Maternal SES and child mental health share aetiological overlap such that shared genetic influence was greater at the lower end of the socioeconomic distribution. Our findings collectively highlight the role that family socioeconomic factors play in shaping the origins of child emotional and behavioural problems., (© 2023 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Background: Low socioeconomic status is a risk factor for depression. The nature and magnitude of associations can differ cross-culturally and is influenced by a range of contextual factors. We examined the aetiology of socioeconomic indicators and depression symptoms and investigated whether socioeconomic indicators moderate genetic and environmental influences on depression symptoms in a Sri Lankan population., Methods: Data were from a population-based sample of twins (N = 2934) and singletons (N = 1035) in Colombo, Sri Lanka. Standard of living, educational attainment, and financial strain were used to index socioeconomic status. Depression symptoms were assessed using the Revised Beck Depression Inventory. Structural equation modelling explored genetic and environmental influences on socioeconomic indicators and depression symptoms and moderation of aetiological influences on depression symptoms by socioeconomic status., Results: Depression symptoms were associated with lower standard of living, lower educational attainment, and financial strain. Sex differences were evident in the aetiology of standard of living, with a small contribution of genetic influences in females. Educational attainment was moderately heritable in both males and females. Total variance in depression was greater among less socioeconomically advantaged individuals. Modest evidence of moderation of the aetiology of depression by standard of living and education was observed., Limitations: While the sample is representative of individuals living in Colombo District, it may not be representative of different regions of Sri Lanka., Conclusions: The aetiology of depression varies across socioeconomic contexts, suggesting a potential mechanism through which socioeconomic disadvantage increases the risk for depression in Sri Lanka. Findings have implications for cross-cultural investigations of the role of socioeconomic factors in depression and for identifying targets for social interventions., Competing Interests: Declaration of competing interest Matthew Hotopf declares research funding from Innovative Medicines Initiative (European Commission), Janssen, Lundbeck, MSD, Biogen and UCB. All other authors declare no competing interests., (Copyright © 2023. Published by Elsevier B.V.)

Identifying early causal factors leading to the development of poor mental health and behavioral outcomes is essential to design efficient preventive interventions. The substantial associations observed between parental risk factors (e.g., maternal stress in pregnancy, parental education, parental psychopathology, parent-child relationship) and child outcomes point toward the importance of parents in shaping child outcomes. However, such associations may also reflect confounding, including genetic transmission-that is, the child inherits genetic risk common to the parental risk factor and the child outcome. This can generate associations in the absence of a causal effect. As randomized trials and experiments are often not feasible or ethical, observational studies can help to infer causality under specific assumptions. This review aims to provide a comprehensive summary of current causal inference methods using observational data in intergenerational settings. We present the rich causal inference toolbox currently available to researchers, including genetically informed and analytical methods, and discuss their application to child mental health and related outcomes. We outline promising research areas and discuss how existing approaches can be combined or extended to probe the causal nature of intergenerational effects. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Background: In this study we compare results obtained when applying the monozygotic twin difference cross-lagged panel model (MZD-CLPM) and a random intercept cross-lagged panel model (RI-CLPM) to the same data. Each of these models is designed to strengthen researchers' ability to draw causal inference from cross-lagged associations. We explore differences and similarities in how each model does this, and in the results each model produces. Specifically, we examine associations between maladaptive parenting and child emotional and behavioural problems in identical twins aged 9, 12 and 16., Method: Child reports of 5698 identical twins from the Twins Early Development Study (TEDS) were analysed. We ran a regular CLPM to anchor our findings within the current literature, then applied the MZD-CLPM and the RI-CLPM., Results: The RI-CLPM and MZD-CLPM each enable researchers to evaluate the direction of effects between correlated variables, after accounting for unmeasured sources of potential confounding. Our interpretation of these models therefore focusses primarily on the magnitude and significance of cross-lagged associations. In both the MZD-CLPM and the RI-CLPM behavioural problems at age 9 resulted in higher levels of maladaptive parenting at age 12. Other effects were not consistently significant across the two models, although the majority of estimates pointed in the same direction., Conclusion: In light of the triangulated methods, differences in the results obtained using the MZD-CLPM and the RI-CLPM underline the importance of careful consideration of what sources of unmeasured confounding different models control for and that nuance is required when interpreting findings using such models. We provide an overview of what the CLPM, RI-CLPM and MZD-CLPM can and cannot control for in this respect and the conclusions that can be drawn from each model., Competing Interests: Tom A. McAdams is on the JCPP Advances Editorial Advisory Board. The remaining authors have declared that they have no competing or potential conflicts of interest., (© 2023 The Authors. JCPP Advances published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Background: Several longitudinal studies have cast doubt on the aetiological overlap between child and adult attention-deficit hyperactivity disorder (ADHD). However, a lack of genetically sensitive data following children across adulthood precludes direct evaluation of aetiological overlap between child and adult ADHD., Aims: We circumvent the existing gap in longitudinal data by exploring genetic overlap between maternal (adult) and offspring (child) ADHD and comorbid symptoms in an extended family cohort., Method: Data were drawn from the Norwegian Mother, Father and Child Cohort Study, a Norwegian birth registry cohort of 114 500 children and their parents. Medical Birth Registry of Norway data were used to link extended families. Mothers self-reported their own ADHD symptoms when children were aged 3 years; reported children's ADHD symptoms at age 5 years; and children's ADHD, oppositional defiant disorder (ODD), conduct disorder, anxiety and depression symptoms at age 8 years. Genetic correlations were derived from Multiple-Children-of-Twins-and-Siblings and extended bivariate twin models., Results: Phenotypic correlations between adult ADHD symptoms and child ADHD, ODD, conduct disorder, anxiety and depression symptoms at age 8 years were underpinned by medium-to-large genetic correlations (child ADHD: r G = 0.55, 95% CI 0.43-0.93; ODD: r G = 0.80, 95% CI 0.46-1; conduct disorder: r G = 0.44, 95% CI 0.28-1; anxiety: r G = 0.72, 95% CI 0.48-1; depression: r G = 1, 95% CI 0.66-1). These cross-generational adult-child genetic correlations were of a comparable magnitude to equivalent child-child genetic correlations with ADHD symptoms at age 5 years., Conclusions: Our findings provide genetically sensitive evidence that ADHD symptoms in adulthood share a common genetic architecture with symptoms of ADHD and four comorbid disorders at age 8 years. These findings suggest that in the majority of cases, ADHD symptoms in adulthood are not aetiologically distinct from in childhood.

Importance: Although selective serotonin reuptake inhibitors (SSRIs) are recommended for postnatal depression treatment, there is a lack of evidence regarding long-term maternal and child outcomes following postnatal SSRI treatment., Objective: To examine whether postnatal SSRI treatment moderated postnatal depression-associated maternal and child outcomes across early childhood years., Design, Setting, and Participants: This cohort study used longitudinal data from the Norwegian Mother, Father and Child Cohort Study. Participating women were recruited in weeks 17 to 18 of pregnancy from 1999 to 2008 and were prospectively followed up after childbirth. Data analysis was performed between December 2021 to October 2022., Exposure: Postnatal depression diagnosis (a binary indicator of eligibility for treatment) was defined as a score of 7 or greater on the 6-item version of the Edinburgh Postnatal Depression Scale. The Hopkins Symptom Checklist was used as a continuous indicator of and postnatal depressive symptomology at postpartum month 6. Postnatal SSRI treatment was identified using self-reported data at postpartum month 6., Main Outcomes and Measures: Maternal outcomes included self-reported depression symptomology and relationship satisfaction from childbirth to postpartum year 5. Child outcomes included maternal-report internalizing and externalizing problems, attention-deficit/hyperactivity disorder symptoms, and motor and language development at ages 1.5, 3, and 5 years. A propensity score adjustment method was used to control for prenatal factors associated with postnatal SSRI exposure probability., Results: Among a total of 61 081 mother-child dyads, 8671 (14.2%) (mean [SD] age, 29.93 [4.76] years) met the criteria for postnatal depression diagnosis, 177 (2.0%) (mean [SD] age, 30.20 [5.01] years) of whom received postnatal SSRI treatment. More severe postnatal depression symptomology was associated with a range of adverse maternal and child outcomes. Focusing analyses only on the postnatal depression dyads indicated that postnatal SSRI treatment attenuated negative associations between postnatal depression and maternal relationship satisfaction at postpartum month 6 (moderation β, 0.13; 95% CI, 0.07-0.19), years 1.5 (moderation β, 0.11; 95% CI, 0.05-0.18) and 3 (moderation β, 0.12; 95% CI, 0.04-0.19), and for child ADHD at age 5 years (moderation β, -0.15; 95% CI, -0.24 to -0.05). Postnatal SSRI treatment mitigated the negative associations between postnatal depression and maternal depression, partner relationship satisfaction, child externalizing problems, and attention-deficit/hyperactivity disorder up to 5 years after childbirth., Conclusions and Relevance: The results of this large prospective cohort study suggest that postnatal SSRI treatment was associated with a reduced risk of postnatal depression-associated maternal mental health problems and child externalizing behaviors across early childhood years. These findings suggest that postnatal SSRI treatment may bring benefits in the long term to women with postnatal depression and their offspring. This study potentially provides valuable information for clinicians and women with postnatal depression to make informed treatment decisions.

Within-family studies typically assess indirect genetic effects of parents on children, however social support theory points to a critical role of partners and children on women's depression. To address this research gap and account for the high heterogeneity of depression, we calculated a general psychiatric factor using eleven major psychiatric polygenic scores (polygenic p), in up to 25,000 parent-offspring trios from the Norwegian Mother, Father and Child Cohort Study (MoBa). Multilevel modeling of trio polygenic p was used to distinguish direct and indirect genetic effects on mothers depression during pregnancy (gestational age 17 and 30 weeks), infancy (6 months, 18 months) and early childhood (3 years, 5 years, and 8 years). We found mothers polygenic p predicts their depression symptoms (b = 0.092; 95 % CI [0.087,0.098]), outperforming prediction using a single major depressive disorder polygenic score (b = 0.070, 95 % CI [0.066,0.075]). Jointly modeling trio polygenic p revealed indirect genetic effects of fathers (b = 0.022, 95 % CI [0.014,0.030]) and children (b = 0.021, 95 % CI [0.010,0.037]) on mothers' depression. Our results support the generalizability of polygenic effects across mental health and highlight the role of close family members on women's depression., Competing Interests: Conflict of interest We declare no competing conflicts of interests in relation to the submitted work., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Child temperament traits and mothers' emotional symptoms relating to anxiety and depression may drive changes in one another, leading to their 'co-development' across time. Alternatively, links between mother and child traits may be attributable to shared genetic propensities. We explored longitudinal associations between mothers' emotional symptoms and child temperament traits and adjusted for genetic effects shared across generations., Methods: This study is based on the Norwegian Mother, Father and Child Cohort Study (MoBa). Mothers ( n  = 34,060) reported on their symptoms of anxiety and depression, and temperament among offspring ( n  = 42,526), at child ages 1.5, 3 and 5 years. Structural equation models parameterised developmental change in traits, and an extended family design adjusted for genetic effects., Results: We found individual differences in stable trait scores and rate of change for all study variables. Longitudinal stability in mothers' emotional symptoms was associated with longitudinal stability in offspring emotionality ( r  = 0.143), shyness ( r  = 0.031), and sociability ( r  = -0.015). Longitudinal change in mothers' symptoms showed very small or negligible correlations with longitudinal change in child temperament. Both genetic and environmental influences explained the stable longitudinal association between mothers' symptoms and child emotionality., Conclusions: The studied associations between mother and child traits across time appeared to be due to stable, trait-like factors, involving genetic and environmental influence, rather than their co-development. Findings contribute knowledge on how emotional symptoms develop in families across time, and the methods with which we can explore such development., Competing Interests: Eivind Ystrom is a Joint Editor for JCPP Advances. Tom McAdams serves on the JCPP Advances Editorial Advisory Board. The remaining authors have declared that they have no competing or potential conflicts of interest., (© 2023 The Authors. JCPP Advances published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Distinguishing between the effects of nature and nurture constitutes a major research goal for those interested in understanding human development. It is known, for example, that many parent traits predict mental health outcomes in children, but the causal processes underlying such associations are often unclear. Family-based quasi-experimental designs such as sibling comparison, adoption and extended family studies have been used for decades to distinguish the genetic transmission of risk from the environmental effects family members potentially have on one another. Recently, these designs have been combined with genomic data, and this combination is fuelling a range of exciting methodological advances. In this review we explore these advances - highlighting the ways in which they have been applied to date and considering what they are likely to teach us in the coming years about the aetiology and intergenerational transmission of psychopathology., (© 2022 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

The Twins Early Development Study (TEDS) is a longitudinal study following a cohort of twins born 1994-1996 in England and Wales. Of the 13,759 families who originally consented to take part, over 10,000 families remain enrolled in the study. The current focus of TEDS is on mental health in the mid-twenties. Making use of over 25 years of genetically sensitive data, TEDS is uniquely placed to explore the longitudinal genetic and environmental influences on common mental health disorders in early adulthood. This paper outlines recent data collection efforts supporting this work, including a cohort-wide mental health assessment at age 26 and a multi-phase Covid-19 study. It will also provide an update on data linkage efforts and the Children of TEDS (CoTEDS) project., Competing Interests: No authors have declared any competing or potential conflicts of interest., (© 2023 The Authors. JCPP Advances published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Background: Theoretical models of the development of childhood externalizing disorders emphasize the role of parents. Empirical studies have not been able to identify specific aspects of parental behaviors explaining a considerable proportion of the observed individual differences in externalizing problems. The problem is complicated by the contribution of genetic factors to externalizing problems, as parents provide both genes and environments to their children. We studied the joint contributions of direct genetic effects of children and the indirect genetic effects of parents through the environment on externalizing problems., Methods: The study used genome-wide single nucleotide polymorphism data from 9,675 parent-offspring trios participating in the Norwegian Mother Father and child cohort study. Based on genomic relatedness matrices, we estimated the contribution of direct genetic effects and indirect maternal and paternal genetic effects on ADHD, conduct and disruptive behaviors at 8 years of age., Results: Models including indirect parental genetic effects were preferred for the ADHD symptoms of inattention and hyperactivity, and conduct problems, but not oppositional defiant behaviors. Direct genetic effects accounted for 11% to 24% of the variance, whereas indirect parental genetic effects accounted for 0% to 16% in ADHD symptoms and conduct problems. The correlation between direct and indirect genetic effects, or gene-environment correlations, decreased the variance with 16% and 13% for conduct and inattention problems, and increased the variance with 6% for hyperactivity problems., Conclusions: This study provides empirical support to the notion that parents have a significant role in the development of childhood externalizing behaviors. The parental contribution to decrease in variation of inattention and conduct problems by gene-environment correlations would limit the number of children reaching clinical ranges in symptoms. Not accounting for indirect parental genetic effects can lead to both positive and negative bias when identifying genetic variants for childhood externalizing behaviors., (© 2022 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Background: Parental criticism is correlated with internalising symptoms in adolescent offspring. This correlation could in part reflect their genetic relatedness, if the same genes influence behaviours in both parents and offspring. We use a Children-of-Twins design to assess whether parent-reported criticism and offspring internalising symptoms remain associated after controlling for shared genes. To aid interpretation of our results and those of previous Children-of-Twins studies, we examine statistical power for the detection of genetic effects and explore the direction of possible causal effects between generations., Methods: Data were drawn from two Swedish twin samples, comprising 876 adult twin pairs with adolescent offspring and 1,030 adolescent twin pairs with parents. Parent reports of criticism towards their offspring were collected concurrently with parent and offspring reports of adolescent internalising symptoms. Children-of-Twins structural equation models were used to control for genetic influence on the intergenerational association between parental criticism and adolescent internalising., Results: Parental criticism was associated with adolescent internalising symptoms after controlling for genetic influence. No significant role was found for shared genes influencing phenotypes in both generations, although power analyses suggested that some genetic effects may have gone undetected. Models could not distinguish directionality for nongenetic, causal effects between generations., Conclusions: Parental criticism may be involved in psychosocial family processes in the context of adolescent internalising. Future studies should seek to identify these processes and provide clarity on the direction of potential causal effects., (© 2021 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Background: Children of parents with high levels of neuroticism tend to have high neuroticism themselves as well as increased risk of experiencing symptoms of anxiety and depression. It is not yet clear how much of this link is attributable to a potential effect of parent on child (e.g., via a socializing effect) versus to shared genetic risk. We aimed to determine whether there is an intergenerational association after accounting for genetic transmission and assortative mating., Methods: We used data from the Norwegian Mother, Father and Child Cohort Study including 11,088 sibling pairs in the parental generation, their partners ( N  = 22,176) and their offspring ( N  = 26,091). Exposures were maternal and paternal neuroticism (self-reported), and the outcomes were neuroticism, symptoms of depression, and symptoms of anxiety in 8-year-old children (mother-reported)., Results: After accounting for assortative mating in parents (phenotypic r  = 0.26) and genetic transmission (explaining 0%-18% of the mother-offspring correlations), potential maternal effects explained 80% (95% CI = 47-95) of the association with offspring neuroticism (mother-child r  = 0.31), 78% (95% CI = 66-89) of the association with offspring depressive symptoms ( r  = 0.31), and 98% (95% CI = 45-112) of the association with offspring anxiety symptoms ( r  = 0.16). Intergenerational transmission of genetic variants associated with paternal neuroticism accounted for ∼40% (CI = 22%-58%) of the father-offspring correlations with neuroticism and symptoms of depression ( r  = 0.13 and 0.13, respectively) but none with offspring symptoms of anxiety ( r  = 0.05). The remaining father-offspring correlations were explained by maternal influences through assortative mating., Conclusions: These results are consistent with direct effects between maternal and offspring neuroticism and between maternal neuroticism and offspring symptoms of anxiety and depression. Further understanding of these intergenerational processes will require an adequate model of how these constructs (neuroticism, anxiety and depression) relate to each other within generations., Competing Interests: Eivind Ystrom is a Joint Editor of JCPP Advances. The remaining authors have declared that they have no competing or potential conflicts of interest. Tom A. McAdams is a member of the JCPP Advances Editorial Advisory Board. [Corrections made on 22 June 2022, after first online publication: This Conflict of Interests statement has been updated in this version.], (© 2021 The Authors. JCPP Advances published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Purpose: On average, boys have lower academic achievement than girls. We investigated whether the timing of puberty is associated with academic achievement, and whether later puberty among boys contributes to the sex difference in academic achievement., Method: Examination scores at age 16 were studied among 13,477 British twins participating in the population-based Twins Early Development Study. A pubertal development scale, a height-based proxy of growth spurt, and age at menarche were used as indicators of puberty. Associations between puberty, sex, and academic achievement were estimated in phenotypic mediation models and biometric twin models., Results: Earlier puberty was associated with higher academic achievement both in boys and girls. The exception was early age at menarche in girls, which associated with lower academic achievement. More than half of the sex differences in academic achievement could be linked to sex differences in pubertal development, but part of this association appeared to be rooted in prepubertal differences. The biometric twin modelling indicated that the association between puberty and academic achievement was due to shared genetic risk factors. Genetic influences on pubertal development accounted for 7%-8% of the phenotypic variation in academic achievement., Conclusions: Pubertal maturation relates to the examination scores of boys and of girls. This can give genes related to pubertal maturation an influence on outcomes in education and beyond. Sex differences in pubertal maturation can explain parts of the sex difference in academic achievement. Grading students when they are immature may not accurately measure their academic potential., (Copyright © 2021 Society for Adolescent Health and Medicine. All rights reserved.)

Objective: The primary aim of the present study was to separate the direct effect of maternal prenatal depression on offspring ADHD from the passive transmission of genetic liability. Method: A children-of-twins and siblings design including 17,070 extended-family units participating in the Norwegian Mother and Child Cohort Study was used. Self-ratings were obtained from parents using the Symptom Checklist during pregnancy. Maternal ratings using Conner's Parent Rating Scale were obtained when the children were 5 years of age. Results: Genetic influences were important for explaining similarity between parents and offspring. There was also evidence for a maternal effect after accounting for genetic transmission ( m = 0.06, 95% confidence interval [CI] = [0.02, 0.09]). Conclusion: Our results were consistent with hypotheses suggesting that maternal prenatal depression influences symptoms of ADHD in offspring. However, the effect was weak and a substantial portion of the association could be accounted for by shared genetic influences.

Children with attention deficit hyperactivity disorder (ADHD) often experience co-occurring emotional problems. ADHD with this comorbidity is associated with poorer outcomes than ADHD without comorbidity. Better understanding of the etiology of comorbidity could improve prevention of negative outcomes for children with ADHD. The sample consisted of 567 twin pairs, 3,632 sibling pairs, and 2,340 cousin pairs from the Norwegian Mother, Father and Child Cohort Study. Mothers rated offspring symptoms of ADHD, anxiety, and depression at 8 years of age. Biometric modeling was performed to examine genetic and environmental contributions to co-occurring symptoms of ADHD and emotional problems in the children. We fitted four variable (inattention, hyperactivity/impulsivity, anxiety, and depression) covariance matrices of additive genetic, common environmental, twin- and individual-specific environmental effects. Genetic, shared environmental, and individual-specific environmental factors contributed to the correlation between ADHD and depression. The pattern was similar for both inattention and hyperactivity/impulsivity. Familial risk factors (genetic and shared environment), but not individual-specific environmental factors contributed to the positive correlations between each of the two ADHD subdomains and anxiety. The genetic contributions to ADHD-depression comorbidity only partly overlapped with genetic contributions to ADHD-anxiety comorbidity. Our findings indicate that shared risk factors for ADHD and comorbid depression were familial as well as individual-specific, while shared risk factors for ADHD and comorbid anxiety were primarily familial. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Objective: Parent anxiety is associated with offspring internalizing problems (emotional problems related to anxiety and depression). This may reflect causal processes, whereby exposure to parent anxiety directly influences offspring internalizing (and/or vice versa). However, parent-offspring associations could also be attributable to their genetic relatedness. A systematic review and meta-analysis were conducted to investigate whether exposure to parent anxiety is associated with offspring internalizing after controlling for genetic relatedness., Method: A literature search across 5 databases identified 429 unique records. Publications were retained if they used a quasi-experimental design in a general population sample to control for participant relatedness in associations between parent anxiety and offspring internalizing outcomes. Publications were excluded if they involved an experimental exposure or intervention. Studies of prenatal and postnatal anxiety exposure were meta-analyzed separately. Pearson's correlation coefficient estimates (r) were pooled using multilevel random-effects models., Results: Eight publications were retained. Data were drawn from 4 population cohorts, each unique to a quasi-experimental design: adoption, sibling-comparison, children-of-twins or in vitro fertilization. Cohorts were located in northern Europe or America. Families were predominantly of European ancestry. Three publications (N families >11,700; offspring age range, 0.5-10 years) showed no association between prenatal anxiety exposure and offspring internalizing outcomes after accounting for participant relatedness (r = .04; 95% CI: -.07, .14). Six publications (N families >12,700; offspring age range, 0.75-22 years) showed a small but significant association between concurrent symptoms in parents and offspring after accounting for participant relatedness (r = .13; 95% CI: .04, .21)., Conclusion: Initial literature, derived from homogeneous populations, suggests that prenatal anxiety exposure does not cause offspring internalizing outcomes. However, postnatal anxiety exposure may be causally associated with concurrent offspring internalizing via nongenetic pathways. Longitudinal stability, child-to-parent effects, and the role of moderators and methodological biases require attention., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

In this review, we discuss how samples comprising monozygotic and dizygotic twin pairs can be used for the purpose of strengthening causal inference by controlling for shared influences on exposure and outcome. We begin by briefly introducing how twin data can be used to inform the biometric decomposition of population variance into genetic, shared environmental, and nonshared environmental influences. We then discuss how extensions to this model can be used to explore whether associations between exposure and outcome survive correction for shared etiology (common causes). We review several analytical approaches that can be applied to twin data for this purpose. These include multivariate structural equation models, cotwin control methods, direction of causation models (cross-sectional and longitudinal), and extended family designs used to assess intergenerational associations. We conclude by highlighting some of the limitations and considerations that researchers should be aware of when using twin data for the purposes of interrogating causal hypotheses., (Copyright © 2021 Cold Spring Harbor Laboratory Press; all rights reserved.)

Indirect genetic effects from relatives may result in misleading quantifications of heritability, but can also be of interest in their own right. In this paper we propose Trio-GCTA, a model for separating direct and indirect genetic effects when genome-wide single nucleotide polymorphism data have been collected from parent-offspring trios. The model is applicable to phenotypes obtained from any of the family members. We discuss appropriate parameter interpretations and apply the method to three exemplar phenotypes: offspring birth weight, maternal relationship satisfaction, and paternal body-mass index, using real data from the Norwegian Mother, Father and Child Cohort Study (MoBa).

Background: Although maternal depressive symptoms are robustly associated with offspring early-life psychopathology symptoms, it is not clear which potential mechanisms are at play. We aimed to estimate the relative importance of genetic transmission and direct environmental exposure in these associations on three occasions in early childhood., Methods: Biometric modeling of maternal sisters and their offspring from the Norwegian Mother and Child Cohort Study. The analyzed sample comprised 22 316 mothers and 35 589 offspring. Mothers reported their own depressive symptoms using the Symptom checklist, and offspring's concurrent symptoms of psychopathology using the Child Behavior Checklist at 1.5, 3, and 5 years postpartum., Results: Associations between maternal symptoms of depression and offspring emotional problems were predominantly explained by passive genetic transmission at 1.5 and 3 years postpartum. At age 5, associations were more due to direct environmental exposure. For offspring behavioral problems, there was no net increase in the importance of direct environmental exposure across occasions., Conclusions: Associations between maternal depressive symptoms and offspring psychopathology symptoms remained after accounting for shared genes, consistent with a small, causal effect. For offspring emotional problems, this effect appeared to increase in importance over time. Our findings imply that treatment of maternal depressive symptoms could also benefit the offspring, and that genetic confounding should be considered in future studies of such mother-offspring associations.

Background: Many studies detect associations between parent behaviour and child symptoms of anxiety and depression. Despite knowledge that anxiety and depression are influenced by a complex interplay of genetic and environmental risk factors, most studies do not account for shared familial genetic risk. Quantitative genetic designs provide a means of controlling for shared genetics, but rely on observed putative exposure variables, and require data from highly specific family structures., Methods: The intergenerational genomic method, Relatedness Disequilibrium Regression (RDR), indexes environmental effects of parents on child traits using measured genotypes. RDR estimates how much the parent genome influences the child indirectly via the environment, over and above effects of genetic factors acting directly in the child. This 'genetic nurture' effect is agnostic to parent phenotype and captures unmeasured heritable parent behaviours. We applied RDR in a sample of 11,598 parent-offspring trios from the Norwegian Mother, Father and Child Cohort Study (MoBa) to estimate parental genetic nurture separately from direct child genetic effects on anxiety and depression symptoms at age 8. We tested for mediation of genetic nurture via maternal anxiety and depression symptoms. Results were compared to a complementary non-genomic pedigree model., Results: Parental genetic nurture explained 14% of the variance in depression symptoms at age 8. Subsequent analyses suggested that maternal anxiety and depression partially mediated this effect. The genetic nurture effect was mirrored by the finding of family environmental influence in our pedigree model. In contrast, variance in anxiety symptoms was not significantly influenced by common genetic variation in children or parents, despite a moderate pedigree heritability., Conclusions: Genomic methods like RDR represent new opportunities for genetically sensitive family research on complex human traits, which until now has been largely confined to adoption, twin and other pedigree designs. Our results are relevant to debates about the role of parents in the development of anxiety and depression in children, and possibly where to intervene to reduce problems.

Background: Low educational attainment in parents is associated with child psychopathology. It is not clear whether the associations are due to risk factors that family members share or due to effects of maternal or paternal education on the offspring. We investigate whether associations between maternal and paternal educational attainment and child symptoms of attention deficit/hyperactivity disorder (ADHD), depression, and academic problems are due to shared genetic factors, shared family environmental factors, or effects of the parental phenotype educational attainment itself., Methods: This study is based on the Norwegian Mother, Father and Child Cohort Study (MoBa). The sample comprised 34,958 children (17,128 girls) in 28,372 extended-family units. We used data from related nuclear families linked by siblings in the parent generation. We applied a quasi-experimental extended children-of-twins design that included siblings in both generations and took account of nonrandom mating by including partners. Educational attainment was self-reported by mothers and fathers. Mothers reported children's symptoms of ADHD, symptoms of depression, and academic problems by questionnaire when the children were 8 years old., Results: Children of lowly educated parents scored higher on all outcomes and had an approximate doubling of the risk of high symptom levels. The association between maternal and paternal educational attainment and child symptoms of ADHD and academic problems persisted after controlling for shared genetic and family environmental factors. Phenotypic transmission to depression was weaker and in the best fitting model fully explained by genetic factors shared by the two generations., Conclusions: Associations between educational attainment of mothers and fathers and child symptoms of ADHD and academic problems could not be ascribed to shared familial risk factors, whereas associations with symptoms of depression could. Parental education or resources and behaviors resulting from low education might be targets of interventions aimed at reducing symptoms of ADHD and academic problems., (© 2020 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Polygenic scores now explain approximately 10% of the variation in educational attainment. However, they capture not only genetic propensity but also information about the family environment. This is because of passive gene-environment correlation, whereby the correlation between offspring and parent genotypes results in an association between offspring genotypes and the rearing environment. We measured passive gene-environment correlation using information on 6,311 adoptees in the UK Biobank. Adoptees' genotypes were less correlated with their rearing environments because they did not share genes with their adoptive parents. We found that polygenic scores were twice as predictive of years of education in nonadopted individuals compared with adoptees ( R 2 s = .074 vs. .037, p = 8.23 × 10 -24 ). Individuals in the lowest decile of polygenic scores for education attained significantly more education if they were adopted, possibly because of educationally supportive adoptive environments. Overall, these results suggest that genetic influences on education are mediated via the home environment.

Do associations between maternal anxiety symptoms and offspring mental health remain after comparing differentially exposed siblings? Participants were 17,724 offspring siblings and 11,553 mothers from the Norwegian Mother and Child Cohort study. Mothers reported anxiety and depressive symptoms at 30 weeks' gestation, and 0.5, 1.5, 3, and 5 years postpartum. Child internalizing and externalizing problems were assessed at ages 1.5, 3, and 5, and modeled using multilevel analyses with repeated measures nested within siblings, nested within mothers. Maternal pre- and postnatal anxiety were no longer associated with child internalizing or externalizing problems after adjusting for maternal depression and familial confounding. Maternal anxiety when the children were in preschool age, however, remained significantly associated with child internalizing but not externalizing problems., (© 2018 Society for Research in Child Development.)

Background: Anxiety in parents is associated with anxiety in offspring, although little is known about the mechanisms underpinning these intergenerational associations. We conducted the first genetically sensitive study to simultaneously examine the effects of mother, father and child anxiety symptoms on each other over time., Method: Adoptive parent and child symptoms were measured at child ages 6, 7 and 8 years from 305 families involved in the Early Growth and Development Study, using a prospective adoption design. Children were adopted at birth to nonrelatives, and composite data on internalising problems within birth families were used as a proxy measure of offspring inherited risk for anxiety. Structural equation models were fitted to the data to examine prospective associations between adoptive mother, father and child symptoms, whilst accounting for individuals' symptom stability over time., Results: Child anxiety symptoms at age 7 predicted adoptive mothers' anxiety symptoms at age 8. No mother-to-child or child-to-father effects were observed. These results were consistent in sensitivity analyses using only paternal offspring reports and using a second measure of child anxiety symptoms. Fathers' anxiety symptoms at child age 6 prospectively predicted child symptoms, but only when paternal offspring reports were included in the model. Composite data on birth family internalising problems were not associated with child anxiety symptoms., Conclusions: Results show environmentally mediated associations between parent and child anxiety symptoms. Results support developmental theories suggesting that child anxiety symptoms can exert influence on caregivers, and mothers and fathers may play unique roles during the development of child symptoms. Further research is needed on the role of genetic transmission associated with anxiety symptoms in biologically related families. In the meantime, researchers and clinicians should strive to include fathers in assessments and consider the effects of child symptoms on caregivers., (© 2019 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

The COllaborative project of Development of Anthropometrical measures in Twins (CODATwins) project is a large international collaborative effort to analyze individual-level phenotype data from twins in multiple cohorts from different environments. The main objective is to study factors that modify genetic and environmental variation of height, body mass index (BMI, kg/m2) and size at birth, and additionally to address other research questions such as long-term consequences of birth size. The project started in 2013 and is open to all twin projects in the world having height and weight measures on twins with information on zygosity. Thus far, 54 twin projects from 24 countries have provided individual-level data. The CODATwins database includes 489,981 twin individuals (228,635 complete twin pairs). Since many twin cohorts have collected longitudinal data, there is a total of 1,049,785 height and weight observations. For many cohorts, we also have information on birth weight and length, own smoking behavior and own or parental education. We found that the heritability estimates of height and BMI systematically changed from infancy to old age. Remarkably, only minor differences in the heritability estimates were found across cultural-geographic regions, measurement time and birth cohort for height and BMI. In addition to genetic epidemiological studies, we looked at associations of height and BMI with education, birth weight and smoking status. Within-family analyses examined differences within same-sex and opposite-sex dizygotic twins in birth size and later development. The CODATwins project demonstrates the feasibility and value of international collaboration to address gene-by-exposure interactions that require large sample sizes and address the effects of different exposures across time, geographical regions and socioeconomic status.

The Children of the Twins Early Development Study (CoTEDS) is a new prospective children-of-twins study in the UK, designed to investigate intergenerational associations across child developmental stages. CoTEDS will enable research on genetic and environmental factors that underpin parent-child associations, with a focus on mental health and cognitive-related traits. Through CoTEDS, we will have a new lens to examine the roles that parents play in influencing child development, as well as the genetic and environmental factors that shape parenting behavior and experiences. Recruitment is ongoing from the sample of approximately 20,000 contactable adult twins who have been enrolled in the Twins Early Development Study (TEDS) since infancy. TEDS twins are invited to register all offspring to CoTEDS at birth, with 554 children registered as of May 2019. By recruiting the second generation of TEDS participants, CoTEDS will include information on adult twins and their offspring from infancy. Parent questionnaire-based data collection is now underway for 1- and 2-year-old CoTEDS infants, with further waves of data collection planned. Current data collection includes the following primary constructs: child mental health, temperament, language and cognitive development; parent mental health and social relationships; parenting behaviors and feelings; and other socioecological factors. Measurement tools have been selected with reference to existing genetically informative cohort studies to ensure overlap in phenotypes measured at corresponding stages of development. This built-in study overlap is intended to enable replication and triangulation of future analyses across samples and research designs. Here, we summarize study protocols and measurement procedures and describe future plans.

This study investigated associations between mindfulness and symptoms of insomnia, depression and anxiety. Mindfulness was disaggregated into five subscales: 'nonreactivity to inner experience', 'observing', 'acting with awareness', 'describing' and 'nonjudging of inner experience'. Twin models were used to examine genetic and environmental influences on mindfulness, symptoms of insomnia, depression and anxiety and on their associations. Data came from a longitudinal twin/sibling study (G1219) comprising 862 individuals (age range 22-32 years, 66% females). Less mindfulness was associated with greater symptoms of insomnia, depression and anxiety (r = .22-.48). Of the mindfulness subscales, 'nonjudging of inner experience' was most strongly associated with the other traits. Overall mindfulness was largely influenced by non-shared environmental factors (E = .72) although familial influences played a role for overall mindfulness, as well as for the 'acting with awareness' and 'describing' subscales. The genetic correlations between overall mindfulness and symptoms of insomnia, depression and anxiety ranged from .32 to .75 (but were non-significant), while the shared environmental correlations ranged from -.78 to .79 (also non-significant). The non-shared environmental influences between these three variables were moderately, significantly correlated (rE = .21-.55)., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The parental feeding practices (PFPs) of excessive restriction of food intake ('restriction') and pressure to increase food consumption ('pressure') have been argued to causally influence child weight in opposite directions (high restriction causing overweight; high pressure causing underweight). However child weight could also 'elicit' PFPs. A novel approach is to investigate gene-environment correlation between child genetic influences on BMI and PFPs. Genome-wide polygenic scores (GPS) combining BMI-associated variants were created for 10,346 children (including 3,320 DZ twin pairs) from the Twins Early Development Study using results from an independent genome-wide association study meta-analysis. Parental 'restriction' and 'pressure' were assessed using the Child Feeding Questionnaire. Child BMI standard deviation scores (BMI-SDS) were calculated from children's height and weight at age 10. Linear regression and fixed family effect models were used to test between- (n = 4,445 individuals) and within-family (n = 2,164 DZ pairs) associations between the GPS and PFPs. In addition, we performed multivariate twin analyses (n = 4,375 twin pairs) to estimate the heritabilities of PFPs and the genetic correlations between BMI-SDS and PFPs. The GPS was correlated with BMI-SDS (β = 0.20, p = 2.41x10-38). Consistent with the gene-environment correlation hypothesis, child BMI GPS was positively associated with 'restriction' (β = 0.05, p = 4.19x10-4), and negatively associated with 'pressure' (β = -0.08, p = 2.70x10-7). These results remained consistent after controlling for parental BMI, and after controlling for overall family contributions (within-family analyses). Heritabilities for 'restriction' (43% [40-47%]) and 'pressure' (54% [50-59%]) were moderate-to-high. Twin-based genetic correlations were moderate and positive between BMI-SDS and 'restriction' (rA = 0.28 [0.23-0.32]), and substantial and negative between BMI-SDS and 'pressure' (rA = -0.48 [-0.52 - -0.44]. Results suggest that the degree to which parents limit or encourage children's food intake is partly influenced by children's genetic predispositions to higher or lower BMI. These findings point to an evocative gene-environment correlation in which heritable characteristics in the child elicit parental feeding behaviour., Competing Interests: The authors have declared that no competing interests exist

Background: Maternal prenatal depression is a known risk factor for early-life psychopathology among offspring; however, potential risk transmission mechanisms need to be distinguished. We aimed to test the relative importance of passive genetic transmission, direct exposure, and indirect exposure in the association between maternal prenatal depressive symptoms and early-life internalising and externalising psychopathology in offspring., Methods: We used structural equation modelling of phenotypic data and genetically informative relationships from the families of participants in the Norwegian Mother and Child Birth Cohort Study (MoBa). The analytic subsample of MoBa used in the current study comprises 22 195 mothers and 35 299 children. We used mothers' self-reported depressive symptoms during pregnancy, as captured by the Symptom Checklist, and their reports of symptoms of psychopathology in their offspring during the first few years of life (measured at 18, 36, and 60 months using the Child Behavior Checklist)., Findings: Maternal prenatal depressive symptoms were found to be associated with early-life psychopathology primarily via intergenerationally shared genetic factors, which explained 41% (95% CI 36-46) of variance in children's internalising problems and 37% (30-44) of variance in children's externalising problems. For internalising problems, phenotypic transmission also contributed significantly, accounting for 14% (95% CI 5-19) of the association, but this contribution was found to be explained by exposure to concurrent maternal depressive symptoms, rather than by direct exposure in utero., Interpretation: Associations between maternal prenatal depressive symptoms and offspring behavioural outcomes in early childhood are likely to be at least partially explained by shared genes. This genetic confounding should be considered when attempting to quantify risks posed by in-utero exposure to maternal depressive symptoms., Funding: UK Economic and Social Research Council, Norwegian Research Council, Norwegian Ministries of Health and Care Services, and Education & Research, Wellcome Trust, Royal Society, and National Institute for Health Research., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Datasets comprising twins and their children can be a useful tool for understanding the nature of intergenerational associations between parent and offspring phenotypes. In the present article we explore structural equation models previously used to analyse Children-of-Twins data, highlighting some limitations and considerations. We then present new variants of these models, showing that extending the models to include multiple offspring per parent addresses several of the limitations discussed. Accompanying the updated models, we provide power calculations and demonstrate with application to simulated data. We then apply to intergenerational analyses of height and weight, using a sub-study of the Norwegian Mother and Child Cohort (MoBa); the Intergenerational Transmission of Risk (IToR) project, wherein all kinships in the MoBa data have been identified (a children-of-twins-and-siblings study). Finally, we consider how to interpret the findings of these models and discuss future directions.

Common genetic influences offer a partial explanation for comorbidity between different psychiatric disorders 1-3 . However, the genetics underlying co-development-the cross-domain co-occurrence of patterns of change over time-of psychiatric symptoms during childhood and adolescence has not been well explored. Here, we show genetic influence on joint symptom trajectories of parent-reported conduct and emotional problems (overall N = 15,082) across development (4-16 years) using both twin- and genome-wide polygenic score analyses (genotyped N = 2,610). Specifically, we found seven joint symptom trajectories, including two characterized by jointly stable and jointly increasing symptoms of conduct and emotional problems, respectively (7.3% of the sample, collectively). Twin modelling analyses revealed substantial genetic influence on trajectories (heritability estimates range of 0.41-0.78). Furthermore, individuals' risk of being classified in the most symptomatic trajectory classes was significantly predicted by polygenic scores for years-of-education-associated alleles and depressive symptoms-associated alleles. Complementary analyses of child self-reported symptoms across late childhood and early adolescence yielded broadly similar results. Taken together, our results indicate that genetic factors are involved in the co-development of conduct and emotional problems across childhood and adolescence, and that individuals with co-developing symptoms across multiple domains may represent a clinical subgroup characterized by increased levels of genetic risk.

Background: Associations between parenting and child outcomes are often interpreted as reflecting causal, social influences. However, such associations may be confounded by genes common to children and their biological parents. To the extent that these shared genes influence behaviours in both generations, a passive genetic mechanism may explain links between them. Here we aim to quantify the relative importance of passive genetic v. social mechanisms in the intergenerational association between parent-offspring relationship quality and offspring internalizing problems in adolescence., Methods: We used a Children-of-Twins (CoT) design with data from the parent-based Twin and Offspring Study of Sweden (TOSS) sample [909 adult twin pairs and their offspring; offspring mean age 15.75 (2.42) years], and the child-based Swedish Twin Study of CHild and Adolescent Development (TCHAD) sample [1120 adolescent twin pairs; mean age 13.67 (0.47) years]. A composite of parent-report measures (closeness, conflict, disagreements, expressions of affection) indexed parent-offspring relationship quality in TOSS, and offspring self-reported internalizing symptoms were assessed using the Child Behavior Checklist (CBCL) in both samples., Results: A social transmission mechanism explained the intergenerational association [r = 0.21 (0.16-0.25)] in our best-fitting model. A passive genetic transmission pathway was not found to be significant, indicating that parental genetic influences on parent-offspring relationship quality and offspring genetic influences on their internalizing problems were non-overlapping., Conclusion: These results indicate that this intergenerational association is a product of social interactions between children and parents, within which bidirectional effects are highly plausible. Results from genetically informative studies of parenting-related effects should be used to help refine early parenting interventions aimed at reducing risk for psychopathology.

For most complex traits, DNA-based heritability ('SNP heritability') is roughly half that of twin-based heritability. A previous report from the Twins Early Development Study suggested that this heritability gap is much greater for childhood behaviour problems than for other domains. If true, this finding is important because SNP heritability, not twin heritability, is the ceiling for genome-wide association studies. With twice the sample size as the previous report, we estimated SNP heritabilities (N up to 4653 unrelated individuals) and compared them with twin heritabilities from the same sample (N up to 4724 twin pairs) for diverse domains of childhood behaviour problems as rated by parents, teachers, and children themselves at ages 12 and 16. For 37 behaviour problem measures, the average twin heritability was 0.52, whereas the average SNP heritability was just 0.06. In contrast, results for cognitive and anthropometric traits were more typical (average twin and SNP heritabilities were 0.58 and 0.28, respectively). Future research should continue to investigate the reasons why SNP heritabilities for childhood behaviour problems are so low compared with twin estimates, and find ways to maximise SNP heritability for genome-wide association studies.

Theoretical models of child development typically consider the home environment as a product of bidirectional effects, with parent- and child-driven processes operating interdependently. However, the developmental structure of these processes during the transition from childhood to adolescence has not been well studied. In this study we used longitudinal genetic analyses of data from 6646 UK-representative twin pairs (aged 9-16 years) to investigate stability and change in parenting and household chaos in the context of parent-child bidirectional effects. Stability in the home environment was modest, arising mainly from parent-driven processes and family-wide influences. In contrast, change over time was more influenced by child-driven processes, indicated by significant age-specific genetic influences. Interpretations of these results and their implications for researchers are discussed., (© 2016 The Authors. Developmental Science Published by John Wiley & Sons Ltd.)

Background: Genes and the environment contribute to variation in adult body mass index [BMI (in kg/m 2 )], but factors modifying these variance components are poorly understood. Objective: We analyzed genetic and environmental variation in BMI between men and women from young adulthood to old age from the 1940s to the 2000s and between cultural-geographic regions representing high (North America and Australia), moderate (Europe), and low (East Asia) prevalence of obesity. Design: We used genetic structural equation modeling to analyze BMI in twins ≥20 y of age from 40 cohorts representing 20 countries (140,379 complete twin pairs). Results: The heritability of BMI decreased from 0.77 (95% CI: 0.77, 0.78) and 0.75 (95% CI: 0.74, 0.75) in men and women 20-29 y of age to 0.57 (95% CI: 0.54, 0.60) and 0.59 (95% CI: 0.53, 0.65) in men 70-79 y of age and women 80 y of age, respectively. The relative influence of unique environmental factors correspondingly increased. Differences in the sets of genes affecting BMI in men and women increased from 20-29 to 60-69 y of age. Mean BMI and variances in BMI increased from the 1940s to the 2000s and were greatest in North America and Australia, followed by Europe and East Asia. However, heritability estimates were largely similar over measurement years and between regions. There was no evidence of environmental factors shared by co-twins affecting BMI. Conclusions: The heritability of BMI decreased and differences in the sets of genes affecting BMI in men and women increased from young adulthood to old age. The heritability of BMI was largely similar between cultural-geographic regions and measurement years, despite large differences in mean BMI and variances in BMI. Our results show a strong influence of genetic factors on BMI, especially in early adulthood, regardless of the obesity level in the population., (© 2017 American Society for Nutrition.)

Study Objectives: Sleep quality is associated with different aspects of psychopathology, but relatively little research has examined links between sleep quality and externalizing behaviors or callous-unemotional traits. We examined: (1) whether an association exists between sleep quality and externalizing behaviors; (2) whether anxiety mediates this association; (3) whether callous-unemotional traits are associated with sleep quality., Methods: Data from two studies were used. Study 1 involved 1556 participants of the G1219 study aged 18-27 years (62% female). Questionnaire measures assessed sleep quality, anxiety, externalizing behaviors, and callous-unemotional traits. Study 2 involved 338 participants aged 18-66 years (65% female). Questionnaires measured sleep quality, externalizing behaviors, and callous-unemotional traits. In order to assess objective sleep quality, actigraphic data were also recorded for a week from a subsample of study 2 participants (n = 43)., Results: In study 1, poorer sleep quality was associated with greater externalizing behaviors. This association was partially mediated by anxiety and moderated by levels of callous-unemotional traits. There was no significant relationship between sleep quality and callous-unemotional traits. In study 2, poorer sleep quality, as assessed via self-reported but not objective measures, was associated with higher levels of externalizing behaviors. Furthermore, in study 2, better sleep quality (indicated in both questionnaires and actigraphy measures: lower mean activity, and greater sleep efficiency) was associated with higher levels of callous-unemotional traits., Conclusions: Self-reports of poorer sleep quality are associated with externalizing behaviors, and this association is partially mediated by anxiety. Callous-unemotional traits are not associated with poor sleep and may even be related to better sleep quality. This is an exceptional finding given that poor sleep quality appears to be a characteristic of most psychopathology., (© Sleep Research Society 2017. Published by Oxford University Press [on behalf of the Sleep Research Society].)

Background: Previous studies have found significant associations between maternal prenatal and postpartum depression and child behavior problems (CBP). The present study investigates whether associations remain in a prospective, longitudinal design adjusted for familial confounding., Methods: The sample comprised 11,599 families including 17,830 siblings from the Norwegian Mother and Child Cohort study. Mothers reported depressive symptoms at gestational weeks 17 and 30, as well as 6 months, 1.5, 3, and 5 years postpartum. Fathers' depression was measured at gestational week 17. At the last three time-points, child internalizing and externalizing problems were concurrently assessed. We performed multilevel analyses for internalizing and externalizing problems separately, using parental depression as predictors. Analyses were repeated using a sibling comparison design to adjust for familial confounding., Results: All parental depressive time-points were significantly and positively associated with child internalizing and externalizing problems. After sibling comparison, however, only concurrent maternal depression was significantly associated with internalizing [estimate = 2.82 (1.91-3.73, 95% CI)] and externalizing problems [estimate = 2.40 (1.56-3.23, 95% CI)]. The effect of concurrent maternal depression on internalizing problems increased with child age., Conclusions: Our findings do not support the notion that perinatal maternal depression is particularly detrimental to children's psychological development, as the most robust effects were found for maternal depression occurring during preschool years., (© 2017 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)