ORCID Profile
0000-0003-4390-6171
Current Organisations
Norwegian Institute of Public Health
,
University of Oslo
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Publisher: Cold Spring Harbor Laboratory
Date: 16-05-2020
DOI: 10.1101/2020.05.15.097840
Abstract: 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 four exemplar phenotypes offspring birth weight, offspring temperament, maternal relationship satisfaction, and paternal body-mass index, using real data from the Norwegian Mother, Father and Child Cohort Study (MoBa).
Publisher: Elsevier BV
Date: 07-2022
DOI: 10.1016/J.JAAC.2021.11.035
Abstract: To investigate the genetic architecture of internalizing symptoms in childhood and adolescence. In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for s le overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument. The meta-analysis of overall internalizing symptoms (INT Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood s les will be key in paving the way to future GWAS success.
Publisher: Elsevier BV
Date: 10-2013
DOI: 10.1016/J.JAAC.2013.07.002
Abstract: Diet quality is related to the risk for depression and anxiety in adults and adolescents however, the possible impact of maternal and early postnatal nutritional exposures on children's subsequent mental health is unexplored. The large prospective Norwegian Mother and Child Cohort Study recruited pregnant women between 1999 and 2008. Data were collected from mothers during pregnancy and when children were 6 months and 1.5, 3, and 5 years of age. Latent growth curve models were used to model linear development in children's internalizing and externalizing problems from 1.5 to 5 years of age as a function of diet quality during pregnancy and at 1.5 and 3 years. Diet quality was evaluated by dietary pattern extraction and characterized as "healthy" or "unhealthy." The s le comprised 23,020 eligible women and their children. Adjustments were made for variables including sex of the child, maternal depression, maternal and paternal age, maternal educational attainment, household income, maternal smoking before and during pregnancy, mothers' parental locus of control, and marital status. Higher intakes of unhealthy foods during pregnancy predicted externalizing problems among children, independently of other potential confounding factors and childhood diet. Children with a high level of unhealthy diet postnatally had higher levels of both internalizing and externalizing problems. Moreover, children with a low level of postnatal healthy diet also had higher levels of both internalizing and externalizing problems. Among this large cohort of mothers and children, early nutritional exposures were independently related to the risk for behavioral and emotional problems in children.
Publisher: Center for Open Science
Date: 25-01-2023
Abstract: Background: We investigate if covariation between parental and child ADHD behaviors can be explained by environmental and/or genetic transmission. Methods: We employed a large children-of-twins-and-siblings s le (N=22,350 parents & 11,566 8-year-old children) of the Norwegian Mother, Father and Child Cohort Study (MoBa). 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 in idual-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.
Publisher: Springer Science and Business Media LLC
Date: 18-03-2023
DOI: 10.1038/S41398-023-02348-Y
Abstract: Parental genes may indirectly influence offspring psychiatric outcomes through the environment that parents create for their children. These indirect genetic effects, also known as genetic nurture, could explain in idual differences in common internalising and externalising psychiatric symptoms during childhood. Advanced statistical genetic methods leverage data from families to estimate the overall contribution of parental genetic nurture effects. This study included up to 10,499 children, 5990 mother–child pairs, and 6,222 father–child pairs from the Norwegian Mother Father and Child Study. Genome-based restricted maximum likelihood (GREML) models were applied using software packages GCTA and M-GCTA to estimate variance in maternally reported depressive, disruptive, and attention-deficit hyperactivity disorder (ADHD) symptoms in 8-year-olds that was explained by direct offspring genetic effects and maternal or paternal genetic nurture. There was no strong evidence of genetic nurture in this s le, although a suggestive paternal genetic nurture effect on offspring depressive symptoms (variance explained (V) = 0.098, standard error (SE) = 0.057) and a suggestive maternal genetic nurture effect on ADHD symptoms (V = 0.084, SE = 0.058) was observed. The results indicate that parental genetic nurture effects could be of some relevance in explaining in idual differences in childhood psychiatric symptoms. However, robustly estimating their contribution is a challenge for researchers given the current paucity of large-scale s les of genotyped families with information on childhood psychiatric outcomes.
Publisher: Wiley
Date: 31-12-2013
Abstract: Knowledge is scarce on what contributes to whether children with early language delay (LD) show persistent, recovering or sometimes late-onset LD without a prior history of early LD in subsequent preschool years. To explore whether an integrative model of vital risk factors, including poor early communication skills, family history of language-related difficulties and male gender, predicts the development of persistent, recovering or late-onset LD trajectories from 3 to 5 years quantitatively and qualitatively differently. LD was assessed by maternal reports on the Ages and Stages Questionnaire at 3 and 5 years for 10 587 children in The Norwegian Mother and Child Cohort Study. Children were classified across time as having no, late onset, transient or persistent LD. Multinomial logistic regression analyses included the integrative model of vital risk factors and covariates. Across time, 3%, 5% and 6.5% of the children displayed persistent, transient and late-onset LD, respectively. The odds for persistent LD were doubled for boys and children with low language comprehension at 1.5 years and tripled by late-talking familial risk. These same odds decreased for transient LD, and even further for late-onset LD. Familial risk for writing and reading difficulties especially increased the odds for late-onset and persistent LD, while familial risk of unintelligible speech increased the odds for transient LD. Although girls had on average far better language comprehension than boys, low language comprehension was a stronger risk factor for persistent LD in girls. Preschool LD trajectories were uniquely predicted from the integrative risk model of poor early communicative skills, family history and male gender. This might benefit identification of different LD trajectories by supporting broader severe vulnerability for persistent LD, milder vulnerability for transient LD, and possibly a specific risk for reading and learning difficulties for children with late-onset LD.
Publisher: Elsevier BV
Date: 06-2017
DOI: 10.1016/J.JOCA.2016.12.015
Abstract: To explore and quantify the relative strengths of the genetic contribution vs the contribution of modifiable environmental factors to severe osteoarthritis (OA) having progressed to total joint arthroplasty. Incident data from the Norwegian Arthroplasty Registry were linked with the Norwegian Twin Registry on the National ID-number in 2014 in a population-based prospective cohort study of same-sex twins born 1915-60 (53.4% females). Education level and height/weight were self-reported and Body Mass Index (BMI) calculated. The total follow-up time was 27 years for hip arthroplasty (1987-2014, 424,914 person-years) and 20 years for knee arthroplasty (1994-2014, 306,207 person-years). We estimated concordances and the genetic contribution to arthroplasty due to OA in separate analyses for the hip and knee joint. The population comprised N = 9058 twin pairs (N = 3803 monozygotic (MZ), N = 5226 dizygotic (DZ)). In total, 73% (95% confidence intervals (CI) = 66-78%) and 45% (95% CI = 30-58%) of the respective variation in hip and knee arthroplasty could be explained by genetic factors. Zygosity (as a proxy for genetic factors) was associated with hip arthroplasty concordance over time when adjusted for sex, age, education and BMI (HR = 2.98, 95% CI = 1.90-4.67 for MZ compared to DZ twins). Knee arthroplasty was to a greater extent dependent on BMI when adjusted for zygosity and the other covariates (HR = 1.15, 95% CI = 1.02-1.29). Hip arthroplasty was strongly influenced by genetic factors whereas knee arthroplasty to a greater extent depended on a high BMI. The study may imply there is a greater potential for preventing progression of knee OA to arthroplasty in comparison with hip OA.
Publisher: American Psychological Association (APA)
Date: 06-2022
DOI: 10.1037/ADB0000681
Publisher: Center for Open Science
Date: 13-08-2022
Abstract: Background: Parents and children resemble each other in ADHD behaviors. A key theoretical postulate from the evolutionary life history theory is that children use information from their environment (e.g., predictability and resource availability) and develop traits that are optimized for future success in that environment. Life history theory therefore expects that variation in children’s ADHD behaviors reflects evolved calibration to the developmental context that parents provide. Alternatively, children may resemble their parents not because of the provided environments, but because of their transmitted genes.Methods: We employed a large children-of-twins-and-siblings s le (N=22,350 parents & 11,566 8-year-old children) of the Norwegian Mother, Father and Child Cohort Study (MoBa). This enables disentangling intergenerational influences via parental genes and parental behavior (i.e., genetic and environmental transmission, respectively). Fathers reported on their symptoms (or absence thereof) and mothers on their own and their child’s symptoms.Results: Child ADHD behaviors correlated 0.24 with ADHD behaviors in mothers and .10 with those in fathers. These correlations were largely due to genetic transmission genetic transmission was five times larger than environmental transmission. Variation in children’s ADHD behaviors was largely explained by heritability (57%), with small effects of parental ADHD behaviors (2% environmental transmission), and gene-environment correlation (3%). The remainder was due to unique environmental influences and noise.Conclusion: The intergenerational transmission of ADHD behaviors is primarily due to genetic transmission, with little evidence for parental ADHD behaviors causing children’s ADHD behaviors. This contradicts the life history theory. The child-specific variability in ADHD behaviors is due, in equal amounts, to genetic factors that influence children’s but not parents’ ADHD behaviors, and to environmental influences and noise that make siblings unique from one another. We conclude that ADHD is not the outcome of adaptive behavior to the (family) environment, but rather a neurodevelopmental disorder with a strong genetic basis.
No related grants have been discovered for Eivind Ystrom.