Bridging temperament and the Big Five in children: A genetically informative study.

Early temperament precedes children's emerging Big Five personality, but shared models of temperament and personality are scarce. We wanted to estimate the genetic factor structure underlying both temperament and the Big Five in children, employing a genetically informed study. Within the Norwegian Mother and Child Cohort Study, we selected 26,354 twins, siblings, and cousins. Mothers rated their children's temperament three times between the ages of 1.5 and 5 years, and the children's Big Five personality at the age of 8. We analyzed the data using biometric modeling. The mean heritability of single-time temperamental traits and Big Five personality traits was .48 and .45, respectively. The mean genetic correlations of temperament across time were .80. The genetic correlations of temperament at 5 years and the Big Five at 8 years revealed two factors, the first comprising reversed Big Five Neuroticism, Agreeableness, Conscientiousness, and reversed EAS Emotionality, the second comprising Big Five Extraversion, Openness to Experience, EAS Activity, Sociability, and reversed Shyness. A confirmatory factor analysis estimated the two factors showing heritabilities of .96 and .72, respectively. The two factors mirrored the metatraits Stability and Plasticity by John M. Digman. Temperament and personality in childhood can be meaningfully bridged using just two metafactors. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Attachment and Political Personality are Heritable and Distinct Systems, and Both Share Genetics with Interpersonal Trust and Altruism.

The attachment and caregiving domains maintain proximity and care-giving behavior between parents and offspring, in a way that has been argued to shape people's mental models of how relationships work, resulting in secure, anxious or avoidant interpersonal styles in adulthood. Several theorists have suggested that the attachment system is closely connected to orientations and behaviors in social and political domains, which should be grounded in the same set of familial experiences as are the different attachment styles. We use a sample of Norwegian twins (N = 1987) to assess the genetic and environmental relationship between attachment, trust, altruism, right-wing authoritarianism (RWA), and social dominance orientation (SDO). Results indicate no shared environmental overlap between attachment and ideology, nor even between the attachment styles or between the ideological traits, challenging conventional wisdom in developmental, social, and political psychology. Rather, evidence supports two functionally distinct systems, one for navigating intimate relationships (attachment) and one for navigating social hierarchies (RWA/SDO), with genetic overlap between traits within each system, and two distinct genetic linkages to trust and altruism. This is counter-posed to theoretical perspectives that link attachment, ideology, and interpersonal orientations through early relational experiences.

Kind of blue - An evaluation of etiologies for prenatal versus postnatal depression symptoms.

BACKGROUND: Prenatal and postnatal depression potentially have severe consequences, but we do not know to what extent they have the same etiological factors. Genetically informative designs yield insight into common etiology between pre- and postnatal depression and inform on potential prevention and intervention efforts. This study evaluates the overlap in genetic and environmental factors in pre- and postnatal depression symptoms. METHODS: We conducted univariate and bivariate modeling, using a quantitative, extended twin study. The sample was a subsample of the MoBa prospective pregnancy cohort study in 6039 pairs of related women. Measurement was conducted at week 30 of pregnancy and 6 months following delivery, using a self-report scale. RESULTS: The heritability of depressive symptoms was 16.2 % (95 % CI = 10.7-22.1) prenatally and 25.7 % (95 % CI = 19.2-32.2) postnatally. The correlation between risk factors for prenatal and postnatal depressive symptoms was at unity (r = 1.00) for genetic effects, and at disunity (r = 0.36) for environmental effects. The genetic effects for postnatal depressive symptoms were 1.7 times larger compared to prenatal depressive symptoms. LIMITATIONS: Although genes for depression become more influential postpartum, only future studies can inform on the mechanisms for such a socio-biological augmentation of effect. CONCLUSION: Genetic risk factors for prenatal and postnatal depressive symptoms are indistinguishable in kind, with greater impact after birth, whereas environmental risk factors for depression symptoms are mostly non-overlapping before and after birth. These findings indicate that interventions could be of different kind before and after birth.

The p factor of psychopathology and personality in middle childhood: genetic and gestational risk factors.

BACKGROUND: A joint, hierarchical structure of psychopathology and personality has been reported in adults but should also be investigated at earlier ages, as psychopathology often develops before adulthood. Here, we investigate the joint factor structure of psychopathology and personality in eight-year-old children, estimate factor heritability and explore external validity through associations with established developmental risk factors. METHODS: Phenotypic and biometric exploratory factor analyses with bifactor rotation on genetically informative data from the Norwegian Mother, Father, and Child Cohort (MoBa) study. The analytic sub-sample comprised 10 739 children (49% girls). Mothers reported their children's symptoms of depression (Short Moods and Feelings Questionnaire), anxiety (Screen for Anxiety Related Disorders), attention-deficit/hyperactivity disorder inattention and hyperactivity, oppositional-defiant disorder, conduct disorder (Parent/Teacher Rating Scale for Disruptive Behavior Disorders), and Big Five personality (short Hierarchical Personality Inventory for Children). Developmental risk factors (early gestational age and being small for gestational age) were collected from the Medical Birth Registry. RESULTS: Goodness-of-fit indices favored a p factor model with three residual latent factors interpreted as negative affectivity, positive affectivity, and antagonism, whereas psychometric indices favored a one-factor model. ADE solutions fitted best, and regression analyses indicated a negative association between gestational age and the p factor, for both the one- and four-factor solutions. CONCLUSION: Correlations between normative and pathological traits in middle childhood mostly reflect one heritable and psychometrically interpretable p factor, although optimal fit to data required less interpretable residual latent factors. The association between the p factor and low gestational age warrants further study of early developmental mechanisms.

Genetic and environmental contributions to co-occurring ADHD and emotional problems in school-aged children.

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).

Associations between maternal depressive symptoms and risk for offspring early-life psychopathology: the role of genetic and non-genetic mechanisms.

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.

Parental Prenatal Symptoms of Depression and Offspring Symptoms of ADHD: A Genetically Informed Intergenerational Study.

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.

Intergenerational transmission of parental neuroticism to emotional problems in 8-year-old children: Genetic and environmental influences.

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.

How important are parents in the development of child anxiety and depression? A genomic analysis of parent-offspring trios in the Norwegian Mother Father and Child Cohort Study (MoBa).

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.

Maternal Drinking and Child Emotional and Behavior Problems.

BACKGROUND AND OBJECTIVES: Maternal drinking is associated with child emotional and behavior problems. There is, however, a lack of studies that properly account for confounding. Our objective was to estimate the association between at-risk drinking in mothers of young children and child emotional and behavior problems, taking into account the passive transmission of familial risk. METHODS: This population-based sample consists of 34 039 children nested within 21 911 nuclear families and 18 158 extended families from the Norwegian Mother, Father, and Child Cohort Study. Participants were recruited between 1999 and 2009 during routine ultrasound examinations. Data were collected during the 17th and 30th gestational week and when the children were 1.5, 3, and 5 years old. We applied a multilevel structural equation model that accounted for unobserved familial risks. RESULTS: Children of mothers with at-risk drinking had a higher likelihood of behavior problems (ß = 3.53; 95% confidence interval [CI] 3.01 to 4.05) than children of mothers with low alcohol consumption. This association was reduced after adjusting for factors in the extended family (ß = 1.93; 95% CI 1.16 to 2.71) and the nuclear family (ß = 1.20; 95% CI 0.39 to 2.01). Maternal at-risk drinking had a smaller association with child emotional problems (ß = 1.80; 95% CI 1.26 to 2.34). This association was reduced after adjusting for factors in the extended family (ß = 0.67; 95% CI -0.12 to 1.46) and the nuclear family (ß = 0.58; 95% CI -0.31 to 1.48). CONCLUSIONS: The results suggest an association between maternal at-risk drinking and child behavior problems. A reduction in maternal drinking may improve outcomes for children with such symptoms.

Mechanisms linking parental educational attainment with child ADHD, depression, and academic problems: a study of extended families in The Norwegian Mother, Father and Child Cohort Study.

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.

Maternal Perinatal and Concurrent Anxiety and Mental Health Problems in Early Childhood: A Sibling-Comparison Study.

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.

A Life Course Study of Genetic and Environmental Influences on Work Incapacity.

Work incapacity is a major public health challenge and an economic burden to both society and individuals. Understanding the underlying causes is becoming ever more relevant as many countries face an aging workforce. We examined stability and change in genetic and environmental factors influencing work incapacity from age 18 until retirement, and sex differences in these effects. The large population-based sample comprised information from 28,759 twins followed for up to 23 years combined with high-quality national registry data. We measured work incapacity as the total proportion of potential workdays lost due to sickness absence, rehabilitation and disability benefits. Structural equation modeling with twin data indicated moderate genetic influences on work incapacity throughout life in both men and women, with a high degree of genetic stability from young to old adulthood. Environmental influences were mainly age-specific. Our results indicate that largely the same genetic factors influence individual differences in work incapacity throughout young, middle and older adulthood, despite major differences in degree of work incapacity and probable underlying medical causes.

Does prenatal stress amplify effects of postnatal maternal depressive and anxiety symptoms on child problem behavior?

Emerging evidence suggests that prenatal stress does not solely undermine child functioning but increases developmental plasticity to both negative and positive postnatal experiences. Here we test this proposition using the Norwegian Mother and Child Cohort study while implementing an extreme-group (i.e., high vs. low prenatal stress) design (n = 27,889 children for internalizing and n = 27,892 for externalizing problems). To measure prenatal stress, mothers reported on depressive and anxiety symptoms at gestational weeks 17 and 30 and of stressful life events at gestational week 30. We then evaluated whether, collectively, such prenatal stress amplified the effect of mothers' postnatal depressive and anxiety symptoms on children's internalizing and externalizing behavior problems at age 5 years. Results showed prenatal stress amplified effects of postnatal maternal depression/anxiety on child internalizing but not externalizing behavior, with some indication that this Prenatal-Stress-×-Postnatal-Maternal-Depression interaction proved more consistent with differential susceptibility than diathesis stress thinking: Children exposed to prenatal stress evinced greater internalizing problems if exposed to more postnatal maternal depressive/anxiety symptoms and, somewhat less strongly, displayed less internalizing problems if they experienced lower postnatal maternal depressive/anxiety symptoms. However, analyses using the whole sample instead of extreme groups yielded opposing results with children exposed to the least prenatal stress evincing greater sensitivity to postnatal maternal depressive/anxiety symptoms with regards to externalizing and internalizing behavior. Taken together, it appears that prenatal stress may have differing effects on plasticity depending on prenatal stress severity. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Is the association between maternal alcohol consumption in pregnancy and pre-school child behavioural and emotional problems causal? Multiple approaches for controlling unmeasured confounding.

BACKGROUND AND AIMS: Hazardous drinking (i.e. alcohol consumption that places drinkers at risk for adverse health outcomes) during pregnancy is associated with adverse child outcomes. To address whether the associations are causal, we aimed to estimate the effect of maternal hazardous drinking during the first trimester on offspring emotional and behavioural problems throughout the pre-school age. We adjusted for: (1) measured confounding (e.g. smoking), (2) familial risk factors by sibling control design and (3) non-shared environmental risk factors by using hazardous drinking the 3 months before pregnancy as an instrumental variable. DESIGN: Prospective cohort study. Participants were recruited between 1999 and 2009 at ultrasound examination offered to all pregnant women in Norway. Data were collected during the 17th and the 30th weeks of gestation, and when the children were aged 1.5, 3 and 5 years. SETTING: Norway, 1999-2015. PARTICIPANTS: The sample consisted of 14 639 mothers with 25 744 offspring siblings from the Norwegian Mother and Child Cohort Study. MEASUREMENTS: Respondents self-reported on: alcohol consumption, children's emotional problems (i.e. emotional reactive, anxiety/depression, somatic complaints) and children's behavioural problems (i.e. attention and aggressive behaviour) throughout pre-school age. We used longitudinal latent growth curve models to estimate the effect of maternal drinking during the first trimester on offspring emotional and behavioural problems. FINDINGS: Most associations were strongly reduced after controlling for both familial and measured environmental risk factors. After adjustment, exposed children were more emotionally reactive [ß = 2.33; 95% confidence interval (CI) = 0.13-4.53] and had more somatic complaints (ß = 1.93; 95% CI = 0.09-3.77) at age 3, but not at age 5. Exposed children were less aggressive than unexposed siblings at age 5 (ß = -2.27; 95% CI = -4.02 to -0.52). CONCLUSIONS: Children exposed to their mothers' hazardous drinking during the first trimester appear to be more emotionally reactive and have more somatic complaints at age 3, but not at age 5, and are less aggressive at age 5 compared with unexposed siblings.

Joint factorial structure of psychopathology and personality.

BACKGROUND: Normative and pathological personality traits have rarely been integrated into a joint large-scale structural analysis with psychiatric disorders, although a recent study suggested they entail a common individual differences continuum. METHODS: We explored the joint factor structure of 11 psychiatric disorders, five personality-disorder trait domains (DSM-5 Section III), and five normative personality trait domains (the 'Big Five') in a population-based sample of 2796 Norwegian twins, aged 19‒46. RESULTS: Three factors could be interpreted: (i) a general risk factor for all psychopathology, (ii) a risk factor specific to internalizing disorders and traits, and (iii) a risk factor specific to externalizing disorders and traits. Heritability estimates for the three risk factor scores were 48% (95% CI 41‒54%), 35% (CI 28‒42%), and 37% (CI 31‒44%), respectively. All 11 disorders had uniform loadings on the general factor (congruence coefficient of 0.991 with uniformity). Ignoring sign and excluding the openness trait, this uniformity of factor loadings held for all the personality trait domains and all disorders (congruence 0.983). CONCLUSIONS: Based on our findings, future research should investigate joint etiologic and transdiagnostic models for normative and pathological personality and other psychopathology.

Development of ADHD symptoms in preschool children: Genetic and environmental contributions.

We examined genetic and environmental contributions to the development of symptoms of attention-deficit/hyperactivity disorder (ADHD) in preschool children. ADHD symptoms in siblings at 1.5, 3, and 5 years of age were investigated in a population-based sample from the prospective Norwegian Mother and Child Cohort Study. The longitudinal contributions of additive genetic, shared, twin-specific, and unique environmental influences were estimated using biometric structural equation models. Heritability of ADHD symptoms ranged from 54% to 70%. There was evidence of partially new genetic influences at successive ages, with genetic correlations ranging from .58 to .89. Contributions from shared environmental factors and twin-specific factors were minor. The importance of unique environmental effects appeared to increase across ages, and was mostly specific to a given age. There was no evidence suggesting that this pattern differs across males and females. Symptoms of ADHD are highly heritability in young children from as early as 1.5 years of age. Longitudinal stability of ADHD symptoms is mainly attributable to genetic influences, but there is also some evidence for age-specific genetic influences. These findings contribute to our understanding of development of ADHD early in life, and can guide future molecular genetics studies.

Maternal prenatal depressive symptoms and risk for early-life psychopathology in offspring: genetic analyses in the Norwegian Mother and Child Birth Cohort Study.

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.