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  • 1
    In: Psychological Medicine, Cambridge University Press (CUP), Vol. 51, No. 3 ( 2021-02), p. 441-449
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0033-2917 , 1469-8978
    RVK:
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2021
    detail.hit.zdb_id: 1470300-2
    SSG: 5,2
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  • 2
    In: Child Development, Wiley, Vol. 91, No. 2 ( 2020-03), p. 456-470
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0009-3920 , 1467-8624
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 215602-7
    detail.hit.zdb_id: 2047406-4
    SSG: 5,2
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  • 3
    In: Journal of Child Psychology and Psychiatry, Wiley, Vol. 63, No. 10 ( 2022-10), p. 1186-1195
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0021-9630 , 1469-7610
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 1470297-6
    SSG: 5,2
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  • 4
    In: Journal of Affective Disorders, Elsevier BV, Vol. 332 ( 2023-07), p. 159-167
    Type of Medium: Online Resource
    ISSN: 0165-0327
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    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 1500487-9
    SSG: 12
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  • 5
    In: European Neuropsychopharmacology, Elsevier BV, Vol. 63 ( 2022-10), p. e169-
    Type of Medium: Online Resource
    ISSN: 0924-977X
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 2019305-1
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  • 6
    In: eLife, eLife Sciences Publications, Ltd, Vol. 12 ( 2023-06-19)
    Abstract: Cortical asymmetry is a ubiquitous feature of brain organization that is subtly altered in some neurodevelopmental disorders, yet we lack knowledge of how its development proceeds across life in health. Achieving consensus on the precise cortical asymmetries in humans is necessary to uncover the developmental timing of asymmetry and the extent to which it arises through genetic and later influences in childhood. Here, we delineate population-level asymmetry in cortical thickness and surface area vertex-wise in seven datasets and chart asymmetry trajectories longitudinally across life (4–89 years; observations = 3937; 70% longitudinal). We find replicable asymmetry interrelationships, heritability maps, and test asymmetry associations in large–scale data. Cortical asymmetry was robust across datasets. Whereas areal asymmetry is predominantly stable across life, thickness asymmetry grows in childhood and peaks in early adulthood. Areal asymmetry is low-moderately heritable (max h 2 SNP ~19%) and correlates phenotypically and genetically in specific regions, indicating coordinated development of asymmetries partly through genes. In contrast, thickness asymmetry is globally interrelated across the cortex in a pattern suggesting highly left-lateralized individuals tend towards left-lateralization also in population-level right-asymmetric regions (and vice versa), and exhibits low or absent heritability. We find less areal asymmetry in the most consistently lateralized region in humans associates with subtly lower cognitive ability, and confirm small handedness and sex effects. Results suggest areal asymmetry is developmentally stable and arises early in life through genetic but mainly subject-specific stochastic effects, whereas childhood developmental growth shapes thickness asymmetry and may lead to directional variability of global thickness lateralization in the population.
    Type of Medium: Online Resource
    ISSN: 2050-084X
    Language: English
    Publisher: eLife Sciences Publications, Ltd
    Publication Date: 2023
    detail.hit.zdb_id: 2687154-3
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  • 7
    In: JCPP Advances, Wiley, Vol. 1, No. 4 ( 2021-12)
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 2692-9384 , 2692-9384
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 3045365-3
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  • 8
    In: Frontiers in Psychology, Frontiers Media SA, Vol. 08 ( 2017-03-31)
    Type of Medium: Online Resource
    ISSN: 1664-1078
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2017
    detail.hit.zdb_id: 2563826-9
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  • 9
    In: Journal of Child Psychology and Psychiatry, Wiley, Vol. 63, No. 10 ( 2022-10), p. 1174-1185
    Abstract: Children with ADHD tend to achieve less than their peers in school. It is unknown whether schools moderate this association. Nonrandom selection of children into schools related to variations in their ADHD risk poses a methodological problem. Methods We linked data on ADHD symptoms of inattention and hyperactivity and parent–child ADHD polygenic scores (PGS) from the Norwegian Mother, Father, and Child Cohort Study (MoBa) to achievement in standardised tests and school identifiers. We estimated interactions of schools with individual differences between students in inattention, hyperactivity, and ADHD‐PGS using multilevel models with random slopes for ADHD effects on achievement over schools. In our PGS analyses, we adjust for parental selection of schools by adjusting for parental ADHD‐PGS (a within‐family PGS design). We then tested whether five school sociodemographic measures explained any interactions. Results Analysis of up to 23,598 students attending 2,579 schools revealed interactions between school and ADHD effects on achievement. The variability between schools in the effects of inattention, hyperactivity and within‐family ADHD‐PGS on achievement was 0.08, 0.07 and 0.05 SDs, respectively. For example, the average effect of inattention on achievement was β = −0.23 ( SE  = 0.009), but in 2.5% of schools with the weakest effects, the value was −0.07 or less. ADHD has a weaker effect on achievement in higher‐performing schools. Schools make more of a difference to the achievements of students with higher levels of ADHD, explaining over four times as much variance in achievement for those with high versus average inattention symptoms. School sociodemographic measures could not explain the ADHD‐by‐school interactions. Conclusions Although ADHD symptoms and genetic risk tend to hinder achievement, schools where their effects are weaker do exist. Differences between schools in support for children with ADHD should be evened out.
    Type of Medium: Online Resource
    ISSN: 0021-9630 , 1469-7610
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 1470297-6
    SSG: 5,2
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  • 10
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2022
    In:  European Journal of Epidemiology Vol. 37, No. 5 ( 2022-05), p. 477-494
    In: European Journal of Epidemiology, Springer Science and Business Media LLC, Vol. 37, No. 5 ( 2022-05), p. 477-494
    Abstract: Several studies have examined maternal health behavior during pregnancy and child outcomes. Negative control variables have been used to address unobserved confounding in such studies. This approach assumes that confounders affect the exposure and the negative control to the same degree. The current study introduces a novel latent variable approach that relaxes this assumption by accommodating repeated measures of maternal health behavior during pregnancy. Methods Monte Carlo simulations were used to examine the performance of the latent variable approach. A real-life example is also provided, using data from the Norwegian Mother, Father, and Child Study (MoBa). Results Simulations: Regular regression analyses without a negative control variable worked poorly in the presence of unobserved confounding. Including a negative control variable improved result substantially. The latent variable approach provided unbiased results in several situations where the other analysis models worked poorly. Real-life data: Maternal alcohol use in the first trimester was associated with increased ADHD symptoms in the child in the standard regression model. This association was not present in the latent variable approach. Conclusion The current study showed that a latent variable approach with a negative control provided unbiased estimates of causal associations between repeated measures of maternal health behavior during pregnancy and child outcomes, even when the effect of the confounder differed in magnitude between the negative control and the exposures. The real-life example showed that inferences from the latent variable approach were incompatible with those from the standard regression approach. Limitations of the approach are discussed.
    Type of Medium: Online Resource
    ISSN: 0393-2990 , 1573-7284
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2004992-4
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