Stability and change in maternal wellbeing and illbeing from pregnancy to three years postpartum.

PURPOSE: Motherhood affects women's mental health, encompassing aspects of both wellbeing and illbeing. This study investigated stability and change in wellbeing (i.e., relationship satisfaction and positive affect) and illbeing (i.e., depressive and anxiety symptoms) from pregnancy to three years postpartum. We further investigated the mutual and dynamic relations between these constructs over time and the role of genetic propensities in their time-invariant stability. DATA AND METHODS: This four-wave longitudinal study included 83,124 women from the Norwegian Mother, Father, and Child Cohort Study (MoBa) linked to the Medical Birth Registry of Norway. Data were collected during pregnancy (30 weeks) and at 6, 18 and 36 months postpartum. Wellbeing and illbeing were based on the Relationship Satisfaction Scale, the Differential Emotions Scale and Hopkins Symptoms Checklist-8. Genetics were measured by the wellbeing spectrum polygenic index. Analyses were based on random intercept cross-lagged panel models using R. RESULTS: All four outcomes showed high stability and were mutually interconnected over time, with abundant cross-lagged predictions. The period of greatest instability was from pregnancy to 6 months postpartum, followed by increasing stability. Prenatal relationship satisfaction played a crucial role in maternal mental health postpartum. Women's genetic propensity to wellbeing contributed to time-invariant stability of all four constructs. CONCLUSION: Understanding the mutual relationship between different aspects of wellbeing and illbeing allows for identifying potential targets for health promotion interventions. Time-invariant stability was partially explained by genetics. Maternal wellbeing and illbeing develop in an interdependent way from pregnancy to 36 months postpartum.

Parental education and children's depression, anxiety, and ADHD traits, a within-family study in MoBa.

Children born to parents with fewer years of education are more likely to have depression, anxiety, and attention-deficit hyperactivity disorder (ADHD), but it is unclear to what extent these associations are causal. We estimated the effect of parents' educational attainment on children's depressive, anxiety, and ADHD traits at age 8 years, in a sample of 40,879 Norwegian children born in 1998-2009 and their parents. We used within-family Mendelian randomization, which employs genetic variants as instrumental variables, and controlled for direct genetic effects by adjusting for children's polygenic indexes. We found little evidence that mothers' or fathers' educational attainment independently affected children's depressive, anxiety, or ADHD traits. However, children's own polygenic scores for educational attainment were independently and negatively associated with these traits. Results suggest that differences in these traits according to parents' education may reflect direct genetic effects more than genetic nurture. Consequences of social disadvantage for children's mental health may however be more visible in samples with more socioeconomic variation, or contexts with larger socioeconomic disparities than present-day Norway. Further research is required in populations with more educational and economic inequality and in other age groups.

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).

Individual differences in internalizing symptoms in late childhood: A variance decomposition into cortical thickness, genetic and environmental differences.

The brain undergoes extensive development during late childhood and early adolescence. Cortical thinning is a prominent feature of this development, and some researchers have suggested that differences in cortical thickness may be related to internalizing symptoms, which typically increase during the same period. However, research has yielded inconclusive results. We utilized a new method that estimates the combined effect of individual differences in vertex-wise cortical thickness on internalizing symptoms. This approach allows for many small effects to be distributed across the cortex and avoids the necessity of correcting for multiple tests. Using a sample of 8763 children aged 8.9 to 11.1 from the ABCD study, we decomposed the total variation in caregiver-reported internalizing symptoms into differences in cortical thickness, additive genetics, and shared family environmental factors and unique environmental factors. Our results indicated that individual differences in cortical thickness accounted for less than 0.5% of the variation in internalizing symptoms. In contrast, the analysis revealed a substantial effect of additive genetics and family environmental factors on the different components of internalizing symptoms, ranging from 06% to 48% and from 0% to 34%, respectively. Overall, while this study found a minimal association between cortical thickness and internalizing symptoms, additive genetics, and familial environmental factors appear to be of importance for describing differences in internalizing symptoms in late childhood. RESEARCH HIGHLIGHTS: We utilized a new method for modelling the total contribution of vertex-wise individual differences in cortical thickness to internalizing symptoms in late childhood. The total contribution of individual differences in cortical thickness accounted for <0.5% of the variance in internalizing symptoms. Additive genetics and shared family environmental variation accounted for 17% and 34% of the variance in internalizing symptoms, respectively. Our results suggest that cortical thickness is not an important indicator for internalizing symptoms in childhood, whereas genetic and environmental differences have a substantial impact.

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.

Genetic similarity between relatives provides evidence on the presence and history of assortative mating.

Assortative mating - the non-random mating of individuals with similar traits - is known to increase trait-specific genetic variance and genetic similarity between relatives. However, empirical evidence is limited for many traits, and the implications hinge on whether assortative mating has started recently or many generations ago. Here we show theoretically and empirically that genetic similarity between relatives can provide evidence on the presence and history of assortative mating. First, we employed path analysis to understand how assortative mating affects genetic similarity between family members across generations, finding that similarity between distant relatives is more affected than close relatives. Next, we correlated polygenic indices of 47,135 co-parents from the Norwegian Mother, Father, and Child Cohort Study (MoBa) and found genetic evidence of assortative mating in nine out of sixteen examined traits. The same traits showed elevated similarity between relatives, especially distant relatives. Six of the nine traits, including educational attainment, showed greater genetic variance among offspring, which is inconsistent with stable assortative mating over many generations. These results suggest an ongoing increase in familial similarity for these traits. The implications of this research extend to genetic methodology and the understanding of social and economic disparities.

The structure of psychiatric comorbidity without selection and assortative mating.

The widespread comorbidity observed across psychiatric disorders may be the result of processes such as assortative mating, gene-environment correlation, or selection into population studies. Between-family analyses of comorbidity are subject to these sources of bias, whereas within-family analyses are not. Because of Mendelian inheritance, alleles are randomly assigned within families, conditional on parental alleles. We exploit this variation to compare the structure of comorbidity across broad psychiatric polygenic scores when calculated either between-family (child polygenic scores) or within-family (child polygenic scores regressed on parental polygenic scores) in over 25,000 genotyped parent-offspring trios from the Norwegian Mother Father and Child Cohort study (MoBa). We fitted a series of factor models to the between- and within-family data, which consisted of a single genetic p-factor and a varying number of uncorrelated subfactors. The best-fitting model was identical for between- and within-family analyses and included three subfactors capturing variants associated with neurodevelopment, psychosis, and constraint, in addition to the genetic p-factor. Partner genetic correlations, indicating assortative mating, were not present for the genetic p-factor, but were substantial for the psychosis (b = 0.081;95% CI [0.038,0.124]) and constraint (b = 0.257;95% CI [0.075,0.439]) subfactors. When average factor levels for MoBa mothers and fathers were compared to a population mean of zero we found evidence of sex-specific participation bias, which has implications for the generalizability of findings from cohort studies. Our results demonstrate the power of the within-family design for better understanding the mechanisms driving psychiatric comorbidity and their consequences on population health.

The genetic underpinnings of right-wing authoritarianism and social dominance orientation explain political attitudes beyond Big Five personality.

OBJECTIVE: Political attitudes are predicted by the key ideological variables of right-wing authoritarianism (RWA) and social dominance orientation (SDO), as well as some of the Big Five personality traits. Past research indicates that personality and ideological traits are correlated for genetic reasons. A question that has yet to be tested concerns whether the genetic variation underlying the ideological traits of RWA and SDO has distinct contributions to political attitudes, or if genetic variation in political attitudes is subsumed under the genetic variation underlying standard Big Five personality traits. METHOD: We use data from a sample of 1987 Norwegian twins to assess the genetic and environmental relationships between the Big Five personality traits, RWA, SDO, and their separate contributions to political policy attitudes. RESULTS: RWA and SDO exhibit very high genetic correlation (r = 0.78) with each other and some genetic overlap with the personality traits of openness and agreeableness. Importantly, they share a larger genetic substrate with political attitudes (e.g., deporting an ethnic minority) than do Big Five personality traits, a relationship that persists even when controlling for the genetic foundations underlying personality traits. CONCLUSION: Our results suggest that the genetic foundations of ideological traits and political attitudes are largely non-overlapping with the genetic foundations of Big Five personality traits.

Genetic and brain similarity independently predict childhood anthropometrics and neighborhood socioeconomic conditions.

Linking the developing brain with individual differences in clinical and demographic traits is challenging due to the substantial interindividual heterogeneity of brain anatomy and organization. Here we employ an integrative approach that parses individual differences in both cortical thickness and common genetic variants, and assess their effects on a wide set of childhood traits. The approach uses a linear mixed model framework to obtain the unique effects of each type of similarity, as well as their covariance. We employ this approach in a sample of 7760 unrelated children in the ABCD cohort baseline sample (mean age 9.9, 46.8% female). In general, associations between cortical thickness similarity and traits were limited to anthropometrics such as height, weight, and birth weight, as well as a marker of neighborhood socioeconomic conditions. Common genetic variants explained significant proportions of variance across nearly all included outcomes, although estimates were somewhat lower than previous reports. No significant covariance of the effects of genetic and cortical thickness similarity was found. The present findings highlight the connection between anthropometrics as well as neighborhood socioeconomic conditions and the developing brain, which appear to be independent from individual differences in common genetic variants in this population-based sample.

More than nature and nurture, indirect genetic effects on children's academic achievement are consequences of dynastic social processes.

Families transmit genes and environments across generations. When parents' genetics affect their children's environments, these two modes of inheritance can produce an 'indirect genetic effect'. Such indirect genetic effects may account for up to half of the estimated genetic variance in educational attainment. Here we tested if indirect genetic effects reflect within-nuclear-family transmission ('genetic nurture') or instead a multi-generational process of social stratification ('dynastic effects'). We analysed indirect genetic effects on children's academic achievement in their fifth to ninth years of schooling in N = 37,117 parent-offspring trios in the Norwegian Mother, Father, and Child Cohort Study (MoBa). We used pairs of genetically related families (parents were siblings, children were cousins; N = 10,913) to distinguish within-nuclear-family genetic-nurture effects from dynastic effects shared by cousins in different nuclear families. We found that indirect genetic effects on children's academic achievement cannot be explained by processes that operate exclusively within the nuclear family.

Examining intergenerational risk factors for conduct problems using polygenic scores in the Norwegian Mother, Father and Child Cohort Study.

The aetiology of conduct problems involves a combination of genetic and environmental factors, many of which are inherently linked to parental characteristics given parents' central role in children's lives across development. It is important to disentangle to what extent links between parental heritable characteristics and children's behaviour are due to transmission of genetic risk or due to parental indirect genetic influences via the environment (i.e., genetic nurture). We used 31,290 genotyped mother-father-child trios from the Norwegian Mother, Father and Child Cohort Study (MoBa), testing genetic transmission and genetic nurture effects on conduct problems using 13 polygenic scores (PGS) spanning psychiatric conditions, substance use, education-related factors, and other risk factors. Maternal or self-reports of conduct problems at ages 8 and 14 years were available for up to 15,477 children. We found significant genetic transmission effects on conduct problems for 12 out of 13 PGS at age 8 years (strongest association: PGS for smoking, ß = 0.07, 95% confidence interval = [0.05, 0.08]) and for 4 out of 13 PGS at age 14 years (strongest association: PGS for externalising problems, ß = 0.08, 95% confidence interval = [0.05, 0.11]). Conversely, we did not find genetic nurture effects for conduct problems using our selection of PGS. Our findings provide evidence for genetic transmission in the association between parental characteristics and child conduct problems. Our results may also indicate that genetic nurture via traits indexed by our polygenic scores is of limited aetiological importance for conduct problems-though effects of small magnitude or effects via parental traits not captured by the included PGS remain a possibility.

Socioeconomic status and risk for child psychopathology: exploring gene-environment interaction in the presence of gene-environment correlation using extended families in the Norwegian Mother, Father and Child Birth Cohort Study.

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.

Genotype-environment interplay in associations between maternal drinking and offspring emotional and behavioral problems.

BACKGROUND: While maternal at-risk drinking is associated with children's emotional and behavioral problems, there is a paucity of research that properly accounts for genetic confounding and gene-environment interplay. Therefore, it remains uncertain what mechanisms underlie these associations. We assess the moderation of associations between maternal at-risk drinking and childhood emotional and behavioral problems by common genetic variants linked to environmental sensitivity (genotype-by-environment [G × E] interaction) while accounting for shared genetic risk between mothers and offspring (GE correlation). METHODS: We use data from 109 727 children born to 90 873 mothers enrolled in the Norwegian Mother, Father, and Child Cohort Study. Women self-reported alcohol consumption and reported emotional and behavioral problems when children were 1.5/3/5 years old. We included child polygenic scores (PGSs) for traits linked to environmental sensitivity as moderators. RESULTS: Associations between maternal drinking and child emotional (ß1 = 0.04 [95% confidence interval (CI) 0.03-0.05]) and behavioral (ß1 = 0.07 [0.06-0.08]) outcomes attenuated after controlling for measured confounders and were almost zero when we accounted for unmeasured confounding (emotional: ß1 = 0.01 [0.00-0.02]; behavioral: ß1 = 0.01 [0.00-0.02]). We observed no moderation of these adjusted exposure effects by any of the PGS. CONCLUSIONS: The lack of strong evidence for G × E interaction may indicate that the mechanism is not implicated in this kind of intergenerational association. It may also reflect insufficient power or the relatively benign nature of the exposure in this sample.

Intergenerational transmission of ADHD behaviors: genetic and environmental pathways.

BACKGROUND: We investigate if covariation between parental and child attention-deficit hyperactivity disorder (ADHD) behaviors can be explained by environmental and/or genetic transmission. METHODS: We employed a large children-of-twins-and-siblings sample (N = 22 276 parents and 11 566 8-year-old children) of the Norwegian Mother, Father and Child Cohort Study. This enabled us to disentangle intergenerational influences via parental genes and parental behaviors (i.e. genetic and environmental transmission, respectively). Fathers reported on their own symptoms and mothers on their own and their child's symptoms. RESULTS: Child ADHD behaviors correlated with their mother's (0.24) and father's (0.10) ADHD behaviors. These correlations were largely due to additive genetic transmission. Variation in children's ADHD behaviors was explained by genetic factors active in both generations (11%) and genetic factors specific to the children (46%), giving a total heritability of 57%. There were small effects of parental ADHD behaviors (2% environmental transmission) and gene-environment correlation (3%). The remaining variability in ADHD behaviors was due to individual-specific environmental factors. CONCLUSIONS: The intergenerational resemblance of ADHD behaviors is primarily due to genetic transmission, with little evidence for parental ADHD behaviors causing children's ADHD behaviors. This contradicts theories proposing environmental explanations of intergenerational transmission of ADHD, such as parenting theories or psychological life-history theory.

Non-random Mating Patterns in Education, Mental, and Somatic Health: A Population Study on Within- and Cross-Trait Associations.

Partners resemble each other on many traits, such as health and education. The traits are usually studied one by one in data from established couples and with potential participation bias. We studied all Norwegian parents who had their first child between 2016 and 2020 (N=187,926) and the siblings of these parents. We analysed grade point averages (GPA), educational attainment (EA), and medical records with prospective diagnostic data on 10 mental and 10 somatic health conditions measured 10 to 5 years before childbirth. We found stronger partner similarity in mental (median r=0.14) than in somatic health conditions (median r=0.04), with ubiquitous cross-trait correlations for mental health conditions (median r=0.13). GPA correlated 0.43 and EA 0.47 between partners. High GPA or EA was associated with better mental (median r=-0.16) and somatic (median r=-0.08) health in partners. Elevated correlations for mental health (median r=0.25) in established couples indicated convergence. Analyses of data on siblings and in-laws revealed deviations from direct assortment, suggesting instead indirect assortment based on related traits. GPA and EA accounted for 30-40% of the partner correlations in health. This has implications for the distribution of risk factors among children and for studies of intergenerational transmission.

Exploring the differentiation of behavioural and emotional problems across childhood: A prospective longitudinal cohort study.

Background: An individual's overall burden of behavioural and emotional problems across childhood is associated with increased likelihood of later mental health conditions. However, the relative extent of behavioural versus emotional problems - that is, the extent to which the domains are differentiated from one another - may provide additional information about who is at risk of developing a mental health condition. Here, we seek to validate differentiation as an independent predictor of later mental health conditions, and to explore its aetiology. Methods: We analysed data from ~79,000 children in the population-based Norwegian Mother, Father, and Child Cohort Study, and linked health-care registries. In preregistered analyses, we modelled the extent and rate of differentiation of behavioural and emotional problems between ages 1.5-5 years, and estimated associations with later symptoms (age 8) and diagnoses (after age 8). We also explored the aetiology of differentiation by estimating associations with early life exposures and, in a subset of 23,945 full siblings, assessing the impact of accounting for unobserved familial confounding. Results: Differentiation of behavioural and emotional problems was associated with later symptoms and diagnoses of mental health conditions, independent of total problems. Maternal at-risk drinking (ß = 0.04 [0.02, 0.06]) and parental relationship problems (ß = 0.04 [0.02, 0.05]) were associated with higher behavioural relative to emotional problems at age 5. Maternal prenatal distress (|ß| = 0.04 [0.03, 0.06]), concurrent distress (|ß| = 0.04 [0.02, 0.06]) and parental education (|ß| = 0.05 [0.04, 0.07]) predicted higher emotional relative to behavioural problems at age 5. Estimates for maternal prenatal distress and at-risk drinking were consistent across both unadjusted and adjusted analyses accounting for unobserved familial risk. Conclusions: Differentiation of behavioural and emotional problems in early childhood represents a valid source of inter-individual variability linked to the later emergence of psychopathology and may be relevant for early detection and prevention strategies for mental health.

Childhood personality and academic performance: A sibling fixed-effects study.

OBJECTIVE: This study investigated the associations between personality traits at age 8 and academic performance between ages 10 and 14, controlling for family confounds. BACKGROUND: Many studies have shown links between children's personality traits and their school performance. However, we lack evidence on whether these associations remain after genetic and environmental confounders are accounted for. METHOD: Sibling data from the Norwegian Mother and Child Cohort Study (MoBa) were used (n = 9701). First, we estimated the overall associations between Big Five personality traits and academic performance, including literacy, numeracy, and foreign language. Second, we added sibling fixed effects to remove unmeasured confounders shared by siblings as well as rating bias. RESULTS: Openness to Experience (between-person ß = 0.22 [95% CI: 0.21-0.24]) and Conscientiousness (between-person ß = 0.18 [95% CI 0.16-0.20]) were most strongly related to educational performance. Agreeableness (between-person ß = 0.06 [95% CI -0.08-0.04]) and Extraversion (between-person ß = 0.02 [95% CI 0.00-0.04]) showed small associations with educational performance. Neuroticism had a moderate negative association (between-person ß = -0.14 [95% CI -0.15-0.11]). All associations between personality and performance were robust to confounding: the within-family estimates from sibling fixed-effects models overlapped with the between-person effects. Finally, childhood personality was equally predictive of educational performance across ages and genders. CONCLUSIONS: Although family background is influential for academic achievement, it does not confound associations with personality. Childhood personality traits reflect unbiased and consistent individual differences in educational potential.

Assessing aetiological overlap between child and adult attention-deficit hyperactivity disorder symptoms in an extended family design.

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: rG = 0.55, 95% CI 0.43-0.93; ODD: rG = 0.80, 95% CI 0.46-1; conduct disorder: rG = 0.44, 95% CI 0.28-1; anxiety: rG = 0.72, 95% CI 0.48-1; depression: rG = 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.

Long-Term Maternal and Child Outcomes Following Postnatal SSRI Treatment.

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 ß, 0.13; 95% CI, 0.07-0.19), years 1.5 (moderation ß, 0.11; 95% CI, 0.05-0.18) and 3 (moderation ß, 0.12; 95% CI, 0.04-0.19), and for child ADHD at age 5 years (moderation ß, -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.