Espen Moen Eilertsen

• Corfield, Elizabeth Claire; Shadrin, Alexey; Frei, Oleksandr; Rahman, Mohammad Zillur; Akdeniz, Bayram Cevdet & Filiz, Tahir Tekin [Show all 29 contributors for this article] (2026). Family genetic designs in MoBa provide insights into health and functioning. Nature. ISSN 0028-0836. doi: 10.1038/s41586-026-10926-5. Full text in Research Archive Show summary

  Genome-wide association studies using large, population-based samples of unrelated individuals have discovered thousands of genetic associations with health and disease1. These studies can help explain genetic and environmental risks. However, increasing evidence suggests that population-based estimates, while precise, can also reflect confounding that affects their use and interpretation. This confounding can be overcome using data from genotyped family members, such as nuclear mother–father–child trios2,3. However, samples of genotyped families are rare4,5,6,7,8,9,10,11. Here we illustrate some of the advantages of familial data using the Norwegian Mother, Father and Child Cohort Study (MoBa), a population-based cohort of parents and offspring with extensive genotype data (n ≈ 230,000) (ref. 3), along with broad and longitudinal phenotyping of health and functioning. We provide an overview of MoBa and describe the quality control of genotype data tailored to this extensively related sample. We then use trio data to illustrate how family-based genomic designs can identify distinct direct and indirect sources of genetic influence and structural confounding. As examples, we analyse children’s height, educational achievement, depressive symptoms and sleep duration. These demonstrations highlight MoBa as a broadly valuable resource for advancing understanding of health and functioning across the lifecourse and generations.

• Demange, Perline Aline Delle; Nivard, Michel G.; Torvik, Fartein Ask; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie & Nordmo, Magnus [Show all 9 contributors for this article] (2026). No evidence of parental mental health influencing children’s academic achievement: a within-family study. European Child and Adolescent Psychiatry. ISSN 1018-8827. doi: 10.1007/s00787-026-03100-9. Full text in Research Archive Show summary

  Children of parents with psychopathology generally perform less well in school than their peers. Parental symptoms might not, however, account for their lower achievement, as other familial factors might contribute. To examine the role of parental symptoms, we analyse data from 9,000 families in the Norwegian Mother, Father, and Child Study (MoBa). Parents reported their symptoms of anxiety, depression, ADHD, eating disorders, and alcohol use disorder during pregnancy and during their child’s childhood. Children in 5th grade (aged 10) completed nationally-standardised tests of mathematics, reading comprehension, and English (as an additional language). Comparing children who are cousins (children-of-siblings design), we controlled for unmeasured factors shared among family members that confound the relationship between parental mental health and children’s academic achievement. We found small associations between greater parental symptoms and lower scores in reading and mathematics (− 0.060 ≤ β ≤ −0.013). However, these associations were no longer significant when comparing cousins whose parents differ in mental health. Results suggest that parental symptoms do not exert a direct, clinically meaningful effect on children’s academic achievement. Although non-significant, associations with parental symptoms measured close to the child’s academic test are less attenuated than those measured during pregnancy. Notably, comparison between the overall MoBa sample and the children-of-siblings samples suggests ascertainment differences that hinder strong generalisations. Our findings underscore the importance of quasi-experimental family designs in identifying modifiable targets in intergenerational health and education research. Supporting parental mental health is crucial but its direct effect on children’s achievement may be smaller than often thought.

• Bond, Tom A.; McAdams, Tom A.; Warrington, Nicole Maree; Hannigan, Laurie; Eilertsen, Espen Moen & Ayorech, Ziada [Show all 12 contributors for this article] (2026). Parental body mass index and offspring childhood body size and eating behaviour: A structural equation modelling analysis in the Norwegian Mother, Father and Child Cohort Study. PLoS Medicine. ISSN 1549-1277. 23(6). doi: 10.1371/journal.pmed.1005094. Full text in Research Archive Show summary

  Background The intergenerational transmission of obesity-related traits could propagate an accelerating cycle of obesity, if parental adiposity causally influences offspring adiposity. The extent to which intergenerational obesity associations are due to such causal effects, as opposed to genetic confounding (inheritance), is unclear. We aimed to establish whether associations between parental peri-pregnancy body mass index (BMI) and offspring birth weight (BW), BMI until 8 years of age, and 8-year-old eating behaviour are due to genetic confounding. Methods and findings Data were from the Norwegian Mother, Father and Child Cohort Study, a prospective population-based birth cohort born between 1999 and 2009 at 50 out of 52 hospital maternity units in Norway. We compared the strength of the associations of maternal pre-pregnancy BMI versus paternal BMI during pregnancy, with offspring outcomes including birth weight and BMI assessed between age 6 months and 8 years of age, and appetite-related eating behaviour traits assessed at age 8 years via the Child Eating Behaviour Questionnaire (CEBQ), adjusting for potential confounders including parity, parental/grandparental language group and parental age, smoking, education and income). We then used an extended children of twins structural equation model (SEM) to quantify the extent to which associations were due to genetic confounding. Up to 85,866 children (51.3% male) were included in linear regression models, whereas SEM models included up to 50,999 children. Maternal BMI was more strongly associated than paternal BMI with offspring BW, but the maternal-paternal difference decreased for offspring BMI after birth. Greater parental BMI was associated with obesity-related offspring eating behaviours. SEM results indicated that genetic confounding did not explain the association between parental BMI and offspring BW, but explained the majority of the association with offspring BMI from 6 months onwards. For 8-year BMI, genetic confounding explained 79% (95% CI [62, 95]; p = 1.9 × 10−12) of the covariance with maternal BMI and 94% (95% CI [72, 113]; p = 2.7 × 10−14) of the covariance with paternal BMI. Limitations of this study include selective recruitment and attrition, potential bias due to parental assortative mating, and that findings may not generalise beyond high-income country settings with high obesity prevalence. Conclusions We found strong evidence that parent–child BMI associations may primarily be due to genetic confounding. When considered alongside prior evidence, this finding may argue against a strong causal effect of maternal or paternal adiposity on childhood adiposity via intrauterine or periconceptional mechanisms.

• Wechsler, Daniel L.; Eilertsen, Espen Moen; Ahmadzadeh, Yasmin I.; Cheesman, Rosa Catherine Gillespie; Adamo, Nicoletta & Hannigan, Laurie [Show all 8 contributors for this article] (2026). Direct and Indirect Genetic Effects on Child ADHD Traits in Early and Mid-Childhood: Trio Genome-Wide Complex Trait Analyses in a Large Norwegian Birth Registry Cohort. Behavior Genetics. ISSN 0001-8244. 56(4), p. 184–193. doi: 10.1007/s10519-026-10273-1. Full text in Research Archive Show summary

  Genetic variants in family members may exert environmentally mediated indirect genetic effects on children’s attention-deficit hyperactivity disorder (ADHD) traits. We set out to quantify the indirect genetic effects of parents’ genotypes on children’s ADHD traits as measured in early and mid-childhood. We analyzed data from genotyped trios of children, mothers, and fathers of European ancestry from the Norwegian Mother, Father and Child Cohort Study (MoBa) birth cohort. Child ADHD data were available for analytic subsamples of 12,374 trios at age 5 (children 50.5% male), and 12,714 trios at age 8 (children 50.9% male). We quantified direct genetic effects of children’s genotype and indirect effects of mothers’ and fathers’ genotypes on children’s ADHD traits at each age. Differing patterns of direct and indirect genetic effects were observed in early and mid-childhood, with predominantly maternal indirect genetic effects on ADHD traits at age 5, and roughly equal direct genetic effects and maternal indirect effects on ADHD traits at age 8. However, large standard errors hindered confident inference as to the relative importance of specific effects, and model fit comparisons ultimately favored models with no indirect genetic effects at age 5 and 8, as well as no direct genetic effects at age 5. We do not find clear evidence of indirect genetic effects of maternal or paternal genotype on child ADHD traits at ages 5 and 8, nor direct genetic effects on child ADHD traits at age 5. While previous findings of indirect genetic effects on ADHD subdomains at ages 3 and 8 broadly support the plausibility of indirect genetic effects operating on total ADHD scores at ages 5 and 8, it appears that indirect genetic effects on overall ADHD trait magnitude may be more difficult to estimate with precision than subdomain-specific effects.

• Porneso, Ralph; Havdahl, Alexandra; Eilertsen, Espen Moen & Ystrom, Eivind (2026). Longitudinal genome-wide analysis reveals putative non-additive loci in trait development. Cell reports. 45(8). doi: 10.1016/j.celrep.2026.117840. Full text in Research Archive Show summary

  Complex traits emerge from reciprocal interactions among genotype, environment, and developmental processes. Yet, standard genetic models assume purely additive effects, potentially obscuring non-additive effects. Here, we introduce a longitudinal log-linear variance and genotype-by-time model to detect associations from within-individual variation departing from additivity, i.e., putative non-additive effects. Applied to early growth (infant length and BMI) and cognitive traits (math and reading) of 45,000 to 65,000 individuals, we report 76 lead putative non-additive loci that are enriched 16-fold for cis-regulatory interactions. Of the 76, 6 overlap prior interaction studies (anthropometric) and only 3 loci overlap prior genome-wide association study (GWAS) (cognitive). Accounting for scale effects and linkage disequilibrium (LD), we observe that additive effects are correlated with putative non-additive effects, i.e., “effect pleiotropy.” These results are consistent with non-additive genetic contribution to trait development, which may partly be absorbed by effects estimated under standard GWAS parameterization that assumes strict additivity.

• Pettersen, Johanne Hagen; Eilertsen, Espen Moen; Hegemann, Laura Elizabeth; Hannigan, Laurie; Lund, Ingunn Olea & Johannessen, Pia Myklebust [Show all 12 contributors for this article] (2026). Intra-familial dynamics of mental distress during the Covid-19 lockdown. Translational Psychiatry. 16(1), p. 1–9. doi: 10.1038/s41398-026-03876-z. Full text in Research Archive Show summary

  Lockdowns and social restrictions imposed in response to the Covid-19 pandemic intensified the proximity and reciprocal exposure among members of nuclear families. It is unclear how variation in mental distress during this period is attributed to potential influences of family members. This study used genetic data from adolescents (n = 4 388), mothers (n = 27 852) and fathers (n = 25 953), to disentangle the contributions of parent-driven, child-driven, and partner-driven components to mental distress during the first two months of the Covid-19 lockdown. Separate models also included adolescents’ non-pandemic mental distress as outcomes (n = 13 484). Trio genome-wide complex trait analyses separated two types of genetic components; direct–how an individual’s genotype is associated with their own mental distress, and indirect–how an individual’s genotype is associated with the mental distress of family members. A trio polygenic score (PGS) design was used to investigate associations of specific genetic liability factors with mental distress, and whether these changed over time (PGS×time). Results suggest that family-level genetic factors contribute to mental distress; variance components capturing indirect genetic effects accounted for 10% of adolescent mental distress (mother-driven), 2–3% of maternal (partner-driven), and 5% of paternal mental distress (child-driven). Mothers’ depression and ADHD PGS were positively associated with fathers’ mental distress. No PGS×time interactions were found. Direct genetic effects accounted for 9–10% variance in mental distress across family members, partly explained by genetic variants associated with anxiety, depression, ADHD and neuroticism. These findings highlight the importance of family dynamics and emphasize the potential value of including family members in mental health interventions.

• Qin, Qi; Cheesman, Rosa Catherine Gillespie; Eilertsen, Espen Moen & Ystrom, Eivind (2026). Children's psychological traits and educational performance: How schools and residential areas moderate how individual traits translate into academic outcomes. JCPP Advances. p. 1–15. doi: 10.1002/jcv2.70100. Full text in Research Archive Show summary

  Abstract Background The extent to which children's psychological traits influence their educational performance is thought to depend on the fit between the individual and their developmental context. However, this assumption has yet to be empirically tested on a population scale. This study examines how neurodevelopmental, mental health, and personality traits interact with latent environmental contexts to enhance, maintain, or mitigate their educational performance. Methods Using the Norwegian Mother, Father and Child Cohort Study (MoBa), we estimated the association between 16 developmental traits and grade point average (GPA) in 26,875 children across environmental contexts in 2131 primary schools, 1075 middle schools, ~14,000 neighborhoods, 1471 districts, and 347 municipalities. Results Across the developmental traits, the effect on GPA ranged from −0.286 to 0.220. However, these effects varied substantially across environmental contexts (SD 0.022 to 0.090). Trait‐by‐context interactions were detected in primary schools (2 traits), middle schools (6 traits), neigbourhoods (0 traits), districts (3 traits), and municipalities (1 trait), respectively. Moderation magnitudes were largest for neurodevelopmental traits in primary schools. On average, the effects of ADHD and communication difficulties were −0.252 and −0.193. However, these effects differed substantially across primary schools with SD 0.090 and 0.070, implying b  < −0.370 and b  < −0.282 in 10% of schools. For average children, primary schools explained 0.504% of middle school GPA. Similarly, the effect of depression and extraversion was dependent on middle‐school environments ( b  = −0.128; SD = 0.058 and b  = 0.024; SD = 0.022). Moreover, schools and districts with high GPAs tended to express lower detrimental effects on children's developmental traits. Conclusion Schools and residential areas function as educational catalysts, enhancing or mitigating the influence of developmental traits. High‐performing environments compensate for psychological challenges, whereas lower‐performing contexts exacerbate difficulties. Because the study integrated multiple traits and contextual levels, the analyses were exploratory and data‐driven, and the findings should be interpreted as hypothesis‐generating. These results suggest a need for both context‐sensitive and individually tailored educational interventions.

• Valstad, Mathias; Eilertsen, Espen Moen; Ayorech, Ziada; Cheesman, Rosa Catherine Gillespie; Demange, Perline Aline Delle & Eftedal, Nikolai Haahjem [Show all 8 contributors for this article] (2026). Indirect genetic effects of siblings. Journal of Child Psychology and Psychiatry. ISSN 0021-9630. doi: 10.1111/jcpp.70130. Full text in Research Archive Show summary

  Background Within-family designs are increasingly used to decompose genotype–trait associations into direct and indirect genetic effects. Many such designs, including trio designs or within-sibship designs, assume an absence of sibling indirect genetic effects. Methods We expand two well-known molecular genetic within-family designs, one variance component (genome-based restricted maximum likelihood) and one trait-based (structural equation modeling with polygenic indices), to estimate sibling indirect genetic effects, along with direct genetic effects. We link the Norwegian Mother, Father, and Child Cohort Study (MoBa) to Norway's national education database to model genetic effects on national standardized testing results at ages 10, 13, and 14, and on parent-rated attention-deficit hyperactivity disorder (ADHD) symptoms at ages 3 and 8 in up to 15,971 genotyped and phenotyped siblings. Results Estimates of direct and indirect genetic effects from the genome-based restricted maximum likelihood and the structural equation modeling with polygenic indices approaches converge, albeit with the variance component estimates typically an order of magnitude greater than the trait-based estimates. We observe no indirect genetic effects of siblings on educational performance at any age, and only slightly negative indirect genetic effects of siblings on ADHD symptoms at age 3. We argue that the latter effect might reflect parental contrasting ratings. Conclusions The results suggest that within-family models of educational performance are unlikely to be drastically biased by an assumption of absent sibling indirect genetic effects. Combining trait-based analyses with variance component analyses can benefit understanding of indirect genetic effects, especially when the effects are not specific to a particular mechanism.

• Eilertsen, Espen Moen; Eftedal, Nikolai Haahjem; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Ebeltoft, Joakim Coleman & Sunde, Hans Fredrik [Show all 9 contributors for this article] (2026). Multivariate maternal effects across the internalizing–externalizing spectrum in childhood: results from the Norwegian mother, father, and child cohort study. Journal of Child Psychology and Psychiatry. ISSN 0021-9630. p. 1–13. doi: 10.1111/jcpp.70111. Full text in Research Archive Show summary

  Background From a functionalist perspective, parenting behaviors have adaptive functions and are partly expressions of genetic variation. Maternal genes that have effects on children are often referred to as indirect maternal genetic effects. Indirect genetic effects provide a means for measuring the role of parenting without the need for specifying the relevant parental behaviors. We studied indirect maternal genetic effects to address both the importance and commonality of parenting across the internalizing–externalizing spectrum of behavior problems in childhood. We further addressed how indirect genetic effects impact our understanding of direct genetic effects if not accounted for. Methods Utilizing data from the Norwegian Mother, Father, and Child Cohort Study (MoBa), our analyses involved 42,423 children and their mothers. Both pedigree and genotype data were used to infer genetic relationships. We applied multivariate latent variable models to distinguish indirect maternal genetic effects and direct offspring genetic effects on seven measures of internalizing–externalizing behaviors. Results Our findings indicate significant maternal genetic influences, explaining 7%–18% of the variance across internalizing–externalizing behaviors. A general maternal effect common across behaviors could adequately account for most of the variability. The analyses further indicate that direct child genetic effects appear smaller and more complex when indirect maternal genetic effects are modeled simultaneously. Conclusions By summarizing the effects of parenting with indirect maternal genetic effects, we show a substantial contribution of parents with respect to internalizing–externalizing behaviors in childhood. Although parenting is multifaceted, the effects of parenting are general and can succinctly be described as a single common dimension. Further, our study demonstrates that direct genetic effects appear smaller and more complex when maternal genetic effects are accounted for, highlighting the confounding potential of parental effects in understanding the role of genetic differences in child psychopathology.

• Eftedal, Nikolai Haahjem; Kleppestø, Thomas Haarklau; Czajkowski, Nikolai Olavi; Eilertsen, Espen Moen; Røysamb, Espen & Vassend, Olav Mandt [Show all 8 contributors for this article] (2026). The Relationship Between Educational Attainment and Right-Wing Authoritarianism: A Discordant Twin Study. Personality and Social Psychology Bulletin. ISSN 0146-1672. doi: 10.1177/01461672251407779. Full text in Research Archive
• Ebeltoft, Joakim Coleman; Ystrøm, Eivind; Ayorech, Ziada & Eilertsen, Espen Moen (2026). Parental wealth and mental disorders in Norway (2006–2023): a nationwide registry-based study of 1.4 million young people. The Lancet Regional Health - Europe. 62. doi: 10.1016/j.lanepe.2025.101567. Full text in Research Archive Show summary

  Background Young people from families with low socioeconomic position have higher rates of mental disorders. However, wealth is underexamined despite large wealth inequity worldwide. Here, we aim to investigate the relationship between early life parental wealth and mental disorders in young Norwegians. Methods We conducted a population study of associations between early-life parental wealth and 17 diagnostic categories of mental disorders in 1.4 M children (7–12), adolescents (13–18), and young adults (19–24) observed 2006–2023. Ranked parental socioeconomic indicators at age 0–6 (wealth, income, occupation, and education) and mental disorder diagnoses (ICD-10 and ICPC-2) were obtained from Norwegian Tax, Employment, Education, and Control and Payment of Health Reimbursements registries. Estimates were derived from mean prevalences, generalised estimating equations, and sibling comparison designs. Findings Parental wealth represents a gradient in young people’s mental disorders across age, sex, diagnostic categories, and cohorts. The lowest wealth quintile demonstrated 87% [95% CI = 78–96%] higher 1-year prevalence than the highest quintile. In multivariable analyses, parental wealth was the strongest predictor of mental disorders relative risk in adolescents (1.83 [1.76–1.9]) and young adults (1.92 [1.8–2.04]), while wealth (1.53 [1.46–1.6]) and education (1.52 [1.45–1.6]) were the strongest predictors in children. Parental wealth has a significant within-family association with mental disorders (relative risks: children 1.57 [1.44–1.71], adolescents 1.34 [1.26–1.42], young adults 1.42 [1.31–1.54]). Interpretation Our study serves as a point of reference for understanding the relationship between parental wealth and mental health. Our findings establish early life parental wealth as a fundamental social gradient in young people’s mental disorders.

• Tamnes, Christian K.; Bekkhus, Mona; Eilertsen, Maja; Nes, Ragnhild Bang; Prydz, Monica Beer & Ystrom, Eivind [Show all 63 contributors for this article] (2025). The nature of the relation between mental well-being and ill-being. Nature Human Behaviour. 9(12), p. 2431–2440. doi: 10.1038/s41562-025-02319-x. Full text in Research Archive
• Norbom, Linn B.; Eilertsen, Espen Moen; Dahl, Andreas; Karl, Valerie; Westlye, Lars Tjelta & Tamnes, Christian K. (2025). Socioeconomic context influences the heritability of child cortical structure. Communications Biology. 8. doi: 10.1038/s42003-025-09022-7. Full text in Research Archive Show summary

  Children differ in brain cortical morphometry and microstructure, which together form the structural foundation for cognition. Cortical structure is highly heritable, but whether heritability varies across socioeconomic status (SES) is unknown. In this preregistered study, we estimated single-nucleotide polymorphism (SNP)-based heritability of cortical thickness, surface area, sulcal depth, and grey-/white-matter contrast (GWC) among 9,080 US 10-year-olds. We then tested whether genetic and environmental contributions were moderated by parental SES, defined as a composite of income, education, and neighbourhood deprivation. Cortical thickness and surface area showed high heritability, while sulcal depth and GWC exhibited moderate heritability. However, among children from lower-SES backgrounds, cortical differences were less genetically related and more uniquely environmentally related, at times exceeding genetic contributions. These findings suggest that in contexts of socioeconomic disadvantage, children’s brain structure reflect lived experience more strongly than previously recognized.

• Gui, Anna; Hollowell, Anja; Wigdor, Emilie M.; Morgan, Morgan J.; Hannigan, Laurie John & Corfield, Elizabeth Claire [Show all 28 contributors for this article] (2025). Genome-wide association meta-analysis of age at onset of walking in over 70,000 infants of European ancestry. Nature Human Behaviour. 9, p. 1470–1487. doi: 10.1038/s41562-025-02145-1. Full text in Research Archive
• Ebeltoft, Joakim Coleman; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Hootegem, Arno Van & Lyngstad, Torkild Hovde [Show all 7 contributors for this article] (2025). The genetic and environmental composition of socioeconomic status in Norway. Nature Communications. 16(1). doi: 10.1038/s41467-025-58961-6. Full text in Research Archive Show summary

  Estimating the contributions of genetic and environmental factors is key to understanding differences in socioeconomic status (SES). However, the heritability of SES varies by measure, method, and context. Here, we estimate genetic and environmental sources of variance and commonality in the ‘big four’ SES indicators. We use high-quality administrative data on educational attainment, occupational prestige, income, and wealth, and employ four family-based and unrelated genotype-based heritability methods, all drawn from the same population-wide cohort of >170,000 Norwegians aged 35-45. By drawing subsamples from a consistent sample and using registry-based data, we reduce differences in estimates due to population characteristics and measurement error. Our results show that genetic variation consistently explains more for educational attainment and occupational prestige. Family-shared environmental contributions explained more for educational attainment and wealth. Our results highlight considerable common influences on the four SES indicators among genetic and shared environmental factors, but not among non-shared environmental factors. Overall, we show how the relative importance of genetic and environmental factors to SES differences in Norway varies by method and type of socioeconomic attainment. This study is a reliable source for comparing heritability methods, and for comparing SES indicators and their genetic and environmental commonality in a social-democratic welfare state.

• Cheesman, Rosa Catherine Gillespie; Anapaz, Ville; Alten, Sjoerd van; Abdellaoui, Abdel; Porneso, Ralph Pascual Ortiz & Ebeltoft, Joakim Coleman [Show all 16 contributors for this article] (2025). Genetic associations with educational fields. Nature Genetics. ISSN 1061-4036. 57, p. 2997–3006. doi: 10.1038/s41588-025-02391-z. Full text in Research Archive Show summary

  Educational field choices shape careers, wellbeing and the societal skill distribution, yet genetic influences on what people study remain poorly understood. Here we show that genetic factors are associated with educational field specializations using genome-wide association studies (GWASs) across 463,134 individuals from Finland, Norway and the Netherlands (effective n between 40,072 and 317,209). We identified 17 independent genome-wide significant variants linked to 7 of 10 educational fields, with average heritability of 7%. The genetic signal is specific to field choice rather than educational level, persisting after controlling for years of schooling and confounding factors. By examining genetic clustering across specializations, we uncovered two key dimensions: technical versus social and practical versus abstract. We performed GWASs of these components and demonstrated distinct genetic correlations with personality, behavior and socioeconomic status. Our findings demonstrate that genomic research can illuminate ‘horizontal’ stratification, revealing insights into vocational interests and social sorting beyond traditional attainment measures.

• Eftedal, Nikolai Haahjem; Eilertsen, Espen Moen; Sunde, Hans Fredrik; Kleppestø, Thomas Haarklau; Ystrøm, Eivind & Czajkowski, Nikolai Olavi (2025). Beyond additive genetic effects: Explaining family resemblance in school performance across millions of pairs of Norwegian relatives. Proceedings of the National Academy of Sciences of the United States of America (PNAS). ISSN 0027-8424. 122(25), p. 1–9. doi: 10.1073/pnas.2419627122. Full text in Research Archive Show summary

  We investigate the hypothesis that family resemblance on school performance can be fully explained by additive genetic effects and assortative mating. Our sample consists of all schoolchildren who took Norwegian national standardized tests between 2007 and 2019 (N = 936,708). These tests measure aptitude in math and reading comprehension, and are taken the years children turn 10, 13, and 14 y old. We identify millions of pairs of relatives within our sample (82 different kinds, in total), including not only conventional biological relatives such as siblings and cousins, but also relatives-in-law, relatives through adoption, twins, and relatives connected through twins. When fitting models which assume that family resemblance arises solely from additive genetic effects and assortative mating, we find that they describe much of our data well, but that they systematically underestimate the similarity of close relatives (particularly monozygotic twins), maternal relatives, relatives-in-law, and relatives through adoption. We discuss potential explanations for these deviations, including shared-environmental effects, nonadditive genetic effects, and gene–environment interplay.

• Hegemann, Laura Elizabeth; Eilertsen, Espen Moen; Pettersen, Johanne Hagen; Corfield, Elizabeth Claire; Cheesman, Rosa Catherine Gillespie & Frach, Leonard [Show all 11 contributors for this article] (2025). Direct and indirect genetic effects on early neurodevelopmental traits. Journal of Child Psychology and Psychiatry. ISSN 0021-9630. 66(7), p. 1053–1064. doi: 10.1111/jcpp.14122. Full text in Research Archive Show summary

  Background Neurodevelopmental conditions are highly heritable. Recent studies have shown that genomic heritability estimates can be confounded by genetic effects mediated via the environment (indirect genetic effects). However, the relative importance of direct versus indirect genetic effects on early variability in traits related to neurodevelopmental conditions is unknown. Methods The sample included up to 24,692 parent-offspring trios from the Norwegian MoBa cohort. We use Trio-GCTA to estimate latent direct and indirect genetic effects on mother-reported neurodevelopmental traits at age of 3 years (restricted and repetitive behaviors and interests, inattention, hyperactivity, language, social, and motor development). Further, we investigate to what extent direct and indirect effects are attributable to common genetic variants associated with autism, ADHD, developmental dyslexia, educational attainment, and cognitive ability using polygenic scores (PGS) in regression modeling. Results We find evidence for contributions of direct and indirect latent common genetic effects to inattention (direct: explaining 4.8% of variance, indirect: 6.7%) hyperactivity (direct: 1.3%, indirect: 9.6%), and restricted and repetitive behaviors (direct: 0.8%, indirect: 7.3%). Direct effects best explained variation in social and communication, language, and motor development (5.1%–5.7%). Direct genetic effects on inattention were captured by PGS for ADHD, educational attainment, and cognitive ability, whereas direct genetic effects on language development were captured by cognitive ability, educational attainment, and autism PGS. Indirect genetic effects on neurodevelopmental traits were primarily captured by educational attainment and/or cognitive ability PGS. Conclusions Results were consistent with differential contributions to neurodevelopmental traits in early childhood from direct and indirect genetic effects. Indirect effects were particularly important for hyperactivity and restricted and repetitive behaviors and interests and may be linked to genetic variation associated with cognition and educational attainment. Our findings illustrate the importance of within-family methods for disentangling genetic processes that influence early neurodevelopmental traits, even when identifiable associations are small.

• Sunde, Hans Fredrik; Eilertsen, Espen Moen & Torvik, Fartein Ask (2025). Understanding indirect assortative mating and its intergenerational consequences for educational attainment. Nature Communications. 16(1), p. 1–14. doi: 10.1038/s41467-025-60483-0. Full text in Research Archive Show summary

  We develop a framework for understanding indirect assortative mating and provide updated definitions of key terms. We then develop family models that use partners of twins and siblings to freely estimate the degree of genetic and social homogamy, and account for it when investigating sources of parent-offspring similarity. We applied the models to educational attainment using 1,545,444 individuals in 212,070 extended families in the Norwegian population and Norwegian Twin Registry. Partner similarity in education was better explained by indirect assortment than direct assortment on observed educational attainment, with social homogamy being particularly important. The implied genotypic partner correlation (r = 0.34) was comparable to earlier studies, and higher than expected under direct assortment. About 38% of the parent-offspring correlation (r = 0.34) was attributable to various forms of environmental transmission. Alternative models that assumed direct assortment estimated environmental transmission to be lower, but these did not fit the data well.

• Sunde, Hans Fredrik; Eilertsen, Espen Moen; Kinge, Jonas Minet; Kleppestø, Thomas Haarklau; Nordmo, Magnus & Caspi, Avshalom [Show all 8 contributors for this article] (2025). Parental income and psychiatric disorders from age 10 to 40: a genetically informative population study. Journal of Child Psychology and Psychiatry. ISSN 0021-9630. 67(1), p. 115–126. doi: 10.1111/jcpp.70022. Full text in Research Archive Show summary

  Background Lower parental income is associated with more psychiatric disorders among offspring, but it is unclear if this association reflects effects of parental income (social causation) or shared risk factors (social selection). Prior research finds contradictory results, which may be due to age differences between the studied offspring. Methods Here, we studied psychiatric disorders in the entire Norwegian population aged 10 to 40 years between 2006 and 2018 (N = 2,468,503). By linking tax registries to administrative health registries, we described prevalence rates by age, sex, and parental income rank. Next, we grouped observations into age groups (adolescence, ages 10–20 years; early adulthood, 21–30 years; adulthood, 30–40 years) and applied kinship-based models with extended families of twins and siblings to decompose the parent–offspring correlation into phenotypic transmission, passive genetic transmission, and passive environmental transmission. Results We found that lower parental income rank was associated with higher prevalence of nearly all psychiatric disorders, except for eating disorders, for both men and women at all ages from 10 to 40 years. Comparing the top with the bottom paternal income quartile, the prevalence ratio of any psychiatric disorder was 0.47 among 10-year-olds and decreased to 0.72 among 40-year-olds. The parent–offspring correlation was −.15 in adolescence, −.10 in early adulthood, and −.06 in adulthood. The kinship-based models indicated that phenotypic transmission could account for 39% of the parent–offspring correlation among adolescents (p < .001), but with no significant contribution in early adulthood (p = .181) or adulthood (p = .737). Passive genetic and environmental transmission contributed to the parent–offspring correlation in all age groups (all p's < .001). Conclusions Our findings are consistent with a significant role of social causation during adolescence, while social selection could fully explain the parent–offspring correlation in adulthood.

• Karl, Valerie Christine; Beck, Dani; Eilertsen, Espen Moen; Morawetz, Carmen; Wiker, Thea & Aksnes, Eira Ranheim [Show all 15 contributors for this article] (2024). Associations between parental psychopathology and youth functional emotion regulation brain networks. Developmental Cognitive Neuroscience. ISSN 1878-9293. 70. doi: 10.1016/j.dcn.2024.101476. Full text in Research Archive Show summary

  Parental mental health is associated with children’s emotion regulation (ER) and risk for psychopathology. The relationship between parental psychopathology and children’s functional ER networks and whether connectivity patterns mediate the relationship between parent and youth psychopathology remains unexplored. Using resting-state functional magnetic resonance imaging data from the Adolescent Brain Cognitive Development Study (N = 4202, mean age = 10.0) and a multilevel approach, we analyzed the relationship between self-reported parental psychopathology and their offsprings’ connectivity of four ER networks, as well as associations with self-reported youth psychopathology at a 3-year follow-up. Parental internalizing and total problems were associated with 1) higher connectivity between a subcortical-cortical integrative and ventrolateral prefrontal cortical (PFC) network, 2) lower connectivity between dorsolateral and ventrolateral PFC networks involved in cognitive aspects of ER, and 3) lower connectivity within a subcortical ER network (β = −0.05–0.04). Parental externalizing and total problems were associated with lower connectivity within the integrative network (βext = −0.05; βtot = −0.04). Mediation analyses yielded direct effects of parental to youth psychopathology, but no mediation effect of ER network connectivity. Overall, our results show that ER network connectivity in youth is related to parental psychopathology, yet do not explain intergenerational transmission of psychopathology.

• Norbom, Linn Bonaventure; Rokicki, Jaroslav; Eilertsen, Espen Moen; Wiker, Thea; Hanson, Jamie & Dahl, Andreas [Show all 13 contributors for this article] (2024). Parental education and income are linked to offspring cortical brain structure and psychopathology at 9–11 years. JCPP Advances. 4(1). doi: 10.1002/jcv2.12220. Full text in Research Archive Show summary

  Background A child's socioeconomic environment can shape central aspects of their life, including vulnerability to mental disorders. Negative environmental influences in youth may interfere with the extensive and dynamic brain development occurring at this time. Indeed, there are numerous yet diverging reports of associations between parental socioeconomic status (SES) and child cortical brain morphometry. Most of these studies have used single metric- or unimodal analyses of standard cortical morphometry that downplay the probable scenario where numerous biological pathways in sum account for SES-related cortical differences in youth. Methods To comprehensively capture such variability, using data from 9758 children aged 8.9–11.1 years from the ABCD Study®, we employed linked independent component analysis (LICA) and fused vertex-wise cortical thickness, surface area, curvature and grey-/white-matter contrast (GWC). LICA revealed 70 uni- and multimodal components. We then assessed the linear relationships between parental education, parental income and each of the cortical components, controlling for age, sex, genetic ancestry, and family relatedness. We also assessed whether cortical structure moderated the negative relationships between parental SES and child general psychopathology. Results Parental education and income were both associated with larger surface area and higher GWC globally, in addition to local increases in surface area and to a lesser extent bidirectional GWC and cortical thickness patterns. The negative relation between parental income and child psychopathology were attenuated in children with a multimodal pattern of larger frontal- and smaller occipital surface area, and lower medial occipital thickness and GWC. Conclusion Structural brain MRI is sensitive to SES diversity in childhood, with GWC emerging as a particularly relevant marker together with surface area. In low-income families, having a more developed cortex across MRI metrics, appears beneficial for mental health.

• Torvik, Fartein Ask; Sunde, Hans Fredrik; Cheesman, Rosa Catherine Gillespie; Eftedal, Nikolai Haahjem; Keller, Matthew C. & Ystrøm, Eivind [Show all 7 contributors for this article] (2024). Non-random mating patterns within and across education and mental and somatic health. Nature Communications. 15(1). doi: 10.1038/s41467-024-54966-9. Full text in Research Archive Show summary

  Partners resemble each other in health and education, but studies usually examine one trait at a time in established couples. Using data from all Norwegian first-time parents (N = 187,926) between 2016–2020, we analyse grade point average at age 16, educational attainment, and medical records of 10 mental and 10 somatic health conditions measured 10 to 5 years before childbirth. We find stronger partner similarity in mental (median r = 0.14) than in somatic health conditions (median r = 0.04), with ubiquitous cross-trait correlations in mental health (median r = 0.13). High grade point average or education is associated with better partner mental (median r = −0.16) and somatic (median r = −0.08) health. Elevated mental health correlations (median r = 0.25) in established couples indicate convergence. Analyses of siblings and in-laws suggest that health similarity is influenced by indirect assortment based on related traits. Adjusting for grade point average or education reduces partner health correlations by 30–40%. These findings have implications for the distribution of risk factors among children, genetic studies, and intergenerational transmission.

• Sunde, Hans Fredrik; Eilertsen, Espen Moen & Torvik, Fartein Ask (2024). Understanding indirect assortative mating and its intergenerational consequences. BioRxiv. ISSN 0362-4331. doi: 10.1101/2024.06.21.600029. Full text in Research Archive
• Vollrath, Margarete E.; Eilertsen, Espen Moen; Torgersen, Svenn Omar; Gjerde, Line Cecilie & Ystrøm, Eivind (2024). Bridging Temperament and the Big Five in Children: A Genetically Informative Study. Journal of Personality and Social Psychology. ISSN 0022-3514. 126(4), p. 660–675. doi: 10.1037/pspp0000500. Full text in Research Archive Show summary

  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.

• Bjørndal, Ludvig Daae; Eilertsen, Espen Moen; Ayorech, Ziada; Cheesman, Rosa; Ahmadzadeh, Yasmin I. & Baldwin, Jessie R. [Show all 13 contributors for this article] (2024). Disentangling direct and indirect genetic effects from partners and offspring on maternal depression using trio-GCTA. Nature Mental Health. 2(4), p. 417–425. doi: 10.1038/s44220-024-00207-3. Full text in Research Archive Show summary

  Maternal depressive symptoms are highly prevalent and can negatively impact affected individuals and family members. Understanding etiological influences on maternal depression, such as genetic liability, is key to inform treatment and prevention efforts. Here we quantified direct and indirect genetic effects (that is, when genetic variants in other individuals influence risk of maternal depression through the environment) from partners and offspring on maternal depressive symptoms at multiple time points using genome-wide complex trait analysis with parent–offspring trios. We used data from the Norwegian Mother, Father and Child cohort study, including up to 21,000 genotyped parent–offspring trios. Models with indirect genetic effects had best fit at three out of five time points (3, 5 and 8 years after birth). The variance in maternal depressive symptoms explained by direct genetic effects ranged from 5% to 14%, whereas indirect genetic effects explained 0–14% of variance across time points. Heritable traits in family members contribute to maternal depressive symptoms through the environment at several time points after birth.

• Dahl, Andreas; Eilertsen, Espen Moen; Cabello, Sara Fernandez Rodriguez; Norbom, Linn B.; Tandberg, Anneli Desire & Leonardsen, Esten [Show all 11 contributors for this article] (2024). Genetic and brain similarity independently predict childhood anthropometrics and neighborhood socioeconomic conditions. Developmental Cognitive Neuroscience. ISSN 1878-9293. 65. doi: 10.1016/j.dcn.2023.101339. Full text in Research Archive Show summary

  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.

• Tandberg, Anneli Desire; Dahl, Andreas; Norbom, Linn Bonaventure; Westlye, Lars Tjelta; Ystrøm, Eivind & Tamnes, Christian Krog [Show all 7 contributors for this article] (2024). Individual differences in internalizing symptoms in late childhood: A variance decomposition into cortical thickness, genetic and environmental differences. Developmental Science. ISSN 1363-755X. 27. doi: 10.1111/desc.13537. Full text in Research Archive Show summary

  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.

• Sunde, Hans Fredrik; Eftedal, Nikolai Haahjem; Cheesman, Rosa; Corfield, Elizabeth C.; Kleppestø, Thomas H. & Seierstad, Anne Caroline [Show all 9 contributors for this article] (2024). Genetic similarity between relatives provides evidence on the presence and history of assortative mating. Nature Communications. 15(1). doi: 10.1038/s41467-024-46939-9. Full text in Research Archive Show summary

  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.

• Ayorech, Ziada; Torvik, Fartein Ask; Cheesman, Rosa; Eilertsen, Espen M.; Valstad, Mathias & Bjørndal, Ludvig Daae [Show all 9 contributors for this article] (2024). The structure of psychiatric comorbidity without selection and assortative mating. Translational Psychiatry. 14(1), p. 1–9. doi: 10.1038/s41398-024-02768-4. Full text in Research Archive
• Gustavson, Kristin; Torvik, Fartein Ask; Smith, George Davey; Røysamb, Espen & Eilertsen, Espen Moen (2024). Familial confounding or measurement error? How to interpret findings from sibling and co-twin control studies. European Journal of Epidemiology (EJE). ISSN 0393-2990. 39, p. 587–603. doi: 10.1007/s10654-024-01132-6. Full text in Research Archive Show summary

  Epidemiological researchers often examine associations between risk factors and health outcomes in non-experimental designs. Observed associations may be causal or confounded by unmeasured factors. Sibling and co-twin control studies account for familial confounding by comparing exposure levels among siblings (or twins). If the exposure-outcome association is causal, the siblings should also differ regarding the outcome. However, such studies may sometimes introduce more bias than they alleviate. Measurement error in the exposure may bias results and lead to erroneous conclusions that truly causal exposure-outcome associations are confounded by familial factors. The current study used Monte Carlo simulations to examine bias due to measurement error in sibling control models when the observed exposure-outcome association is truly causal. The results showed that decreasing exposure reliability and increasing sibling-correlations in the exposure led to deflated exposure-outcome associations and inflated associations between the family mean of the exposure and the outcome. The risk of falsely concluding that causal associations were confounded was high in many situations. For example, when exposure reliability was 0.7 and the observed sibling-correlation was r = 0.4, about 30–90% of the samples (n = 2,000) provided results supporting a false conclusion of confounding, depending on how p-values were interpreted as evidence for a family effect on the outcome. The current results have practical importance for epidemiological researchers conducting or reviewing sibling and co-twin control studies and may improve our understanding of observed associations between risk factors and health outcomes. We have developed an app (SibSim) providing simulations of many situations not presented in this paper.

• Ahmadzadeh, Y. I.; Eilertsen, E. M.; Cheesman, R.; Rayner, C.; Ystrom, E. & Hannigan, L. J. [Show all 7 contributors for this article] (2023). Mothers' symptoms of anxiety and depression and the development of child temperament: A genetically informative, longitudinal investigation. JCPP Advances. 3(4), p. 1–12. doi: 10.1002/jcv2.12171. Full text in Research Archive Show summary

  Background Child temperament traits and mothers' emotional symptoms relating to anxiety and depression may drive changes in one another, leading to their ‘co-development’ across time. Alternatively, links between mother and child traits may be attributable to shared genetic propensities. We explored longitudinal associations between mothers' emotional symptoms and child temperament traits and adjusted for genetic effects shared across generations. Methods This study is based on the Norwegian Mother, Father and Child Cohort Study (MoBa). Mothers (n = 34,060) reported on their symptoms of anxiety and depression, and temperament among offspring (n = 42,526), at child ages 1.5, 3 and 5 years. Structural equation models parameterised developmental change in traits, and an extended family design adjusted for genetic effects. Results We found individual differences in stable trait scores and rate of change for all study variables. Longitudinal stability in mothers' emotional symptoms was associated with longitudinal stability in offspring emotionality (r = 0.143), shyness (r = 0.031), and sociability (r = −0.015). Longitudinal change in mothers' symptoms showed very small or negligible correlations with longitudinal change in child temperament. Both genetic and environmental influences explained the stable longitudinal association between mothers' symptoms and child emotionality. Conclusions The studied associations between mother and child traits across time appeared to be due to stable, trait-like factors, involving genetic and environmental influence, rather than their co-development. Findings contribute knowledge on how emotional symptoms develop in families across time, and the methods with which we can explore such development.

• Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Eilertsen, Espen Moen & Ystrøm, Eivind (2023). Why we need families in genomic research on developmental psychopathology. JCPP Advances. 3(1). doi: 10.1002/jcv2.12138. Full text in Research Archive Show summary

  Background Fundamental questions about the roles of genes, environments, and their interplay in developmental psychopathology have traditionally been the domain of twin and family studies. More recently, the rapidly growing availability of large genomic datasets, composed of unrelated individuals, has generated novel insights. However, there are major stumbling blocks. Only a small fraction of the total genetic influence on childhood psychopathology estimated from family data is captured with measured DNA. Moreover, genetic influence identified using DNA is often confounded with indirect genetic effects of relatives, population stratification and assortative mating. Methods The goal of this paper is to review how combining DNA-based genomic research with family-based quantitative genetics helps to address key issues in genomics and push knowledge further. Results We focus on three approaches to obtaining more accurate and novel genomic findings on the developmental aetiology of psychopathology: (a) using knowledge from twin and family studies, (b) triangulating with twin and family studies, and (c) integrating data and methods with twin and family studies. Conclusion We support the movement towards family-based genomic research, and show that developmental psychologists are particularly well-placed to contribute hypotheses, analysis tools, and data.

• Wiker, Thea; Norbom, Linn B.; Beck, Dani; Agartz, Ingrid; Andreassen, Ole A. & Alnæs, Dag [Show all 14 contributors for this article] (2023). Reaction Time Variability in Children Is Specifically Associated With Attention Problems and Regional White Matter Microstructure. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging. ISSN 2451-9022. 8(8), p. 832–840. doi: 10.1016/j.bpsc.2023.03.010. Full text in Research Archive Show summary

  Background Increased intraindividual variability (IIV) in reaction times (RTs) has been suggested as a key cognitive and behavioral marker of attention problems, but findings for other dimensions of psychopathology are less consistent. Moreover, while studies have linked IIV to brain white matter microstructure, large studies testing the robustness of these associations are needed. Methods We used data from the Adolescent Brain Cognitive Development (ABCD) Study baseline assessment to test the associations between IIV and psychopathology (n = 8622, age = 8.9–11.1 years) and IIV and white matter microstructure (n = 7958, age = 8.9–11.1 years). IIV was investigated using an ex-Gaussian distribution analysis of RTs in correct response go trials in the stop signal task. Psychopathology was measured by the Child Behavior Checklist and a bifactor structural equation model was performed to extract a general p factor and specific factors reflecting internalizing, externalizing, and attention problems. To investigate white matter microstructure, fractional anisotropy, mean diffusivity, axial diffusivity, and radial diffusivity were examined in 23 atlas-based tracts. Results Increased IIV in both short and long RTs was positively associated with the specific attention problems factor (Cohen’s d = 0.13 and d = 0.15, respectively). Increased IIV in long RTs was also positively associated with radial diffusivity in the left and right corticospinal tract (both tracts, d = 0.12). Conclusions Using a large sample and a data-driven dimensional approach to psychopathology, the results provide novel evidence for a small but specific association between IIV and attention problems in children and support previous findings on the relevance of white matter microstructure for IIV.

• Wechsler, Daniel L.; Rijsdijk, Fruhling V.; Adamo, Nicoletta; Eilertsen, Espen Moen; Ahmadzadeh, Yasmin I. & Badini, Isabella [Show all 9 contributors for this article] (2023). Assessing aetiological overlap between child and adult attention-deficit hyperactivity disorder symptoms in an extended family design. BJPsych Open. 9(5), p. 1–7. doi: 10.1192/bjo.2023.554. Full text in Research Archive Show summary

  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.

• Roe, James Michael; Vidal-Piñeiro, Didac; Amlien, Inge; Pan, Mengyu; Sneve, Markus Handal & Schotten, Michel Thiebaut de [Show all 14 contributors for this article] (2023). Tracing the development and lifespan change of population-level structural asymmetry in the cerebral cortex. eLIFE. 12, p. 1–32. doi: 10.7554/eLife.84685. Full text in Research Archive
• Gjerde, Line Cecilie; Eilertsen, Espen Moen; McAdams, Tom A.; Cheesman, Rosa Catherine Gillespie; Moffitt, Terrie & Caspi, Avshalom [Show all 10 contributors for this article] (2023). The p factor of psychopathology and personality in middle childhood: genetic and gestational risk factors. Psychological Medicine. ISSN 0033-2917. 53(9), p. 4275–4285. doi: 10.1017/S0033291723000077. Full text in Research Archive Show summary

  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.

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• Ofstad, Sverre Berg; Peng, Qiyuan; Ebeltoft, Joakim; Bjørndal, Ludvig Daae; Rayner, Christopher & Ayorech, Ziada [Show all 10 contributors for this article] (2026). PGI-by-Environment interactions: practical guidelines for robust research. Full text in Research Archive
• Ystrom, Eivind; Demange, Perline Aline Delle; Cheesman, Rosa Catherine Gillespie; McAdams, Thomas Andrew; Eilertsen, Espen Moen & Timpe, Clara Marie Fides [Show all 8 contributors for this article] (2026). Child Personality Polygenic Indices and Parental Distress: Evidence of Active Gene-Environment Correlations and Interactions from Parent–Offspring Trios. doi: https:/osf.io/fwaqp/overview. Full text in Research Archive Show summary

  Child temperament and personality are conjectured to affect parental distress, and there are findings supporting such transactions. Yet, to date, there is no evidence for such evocative gene-environment correlations using exogenous within-family offspring genetic variation. Using 30 000 parent–offspring genotyped trios from the Norwegian Mother, Father and Child Cohort (MoBa), we test how child personality polygenic indexes (PGIs) independently affect maternal and paternal mental distress across the life course (age 16-60). The second longstanding hypothesis is that such child-to-parent transactions are non-additive due to gene-environment interactions. We will reveal the scope of this by estimating the expansion of within-person-timepoint parental mental distress over child personality PGIs. The third longstanding hypothesis is that the evocative effect is dependent on the parental personality, or the “goodness-of-fit”. We will examine moderation by parental Big Five PGIs to test if the effect of a child’s personality on parent depression depends on the parent’s own personality predispositions. This genetically controlled approach provides a novel and robust test of child- evoked effects across the life course. Results for both mothers and fathers will be presented, highlighting the power of child PGIs as a new tool to reveal intergenerational influences on parental mental distress.

• Ystrom, Eivind; Ayorech, Ziada; Bjørndal, Ludvig Daae; Timpe, Clara Marie Fides; Cheesman, Rosa Catherine Gillespie & Eilertsen, Espen Moen [Show all 8 contributors for this article] (2026). Child Personality Polygenic Indices and Parental Distress: Evidence of Active Gene- Environment Correlations and Interactions from Parent–Offspring Trios. doi: https:/bga.org/docs.ashx?id=1781704. Full text in Research Archive
• Qin, Qi; Demange, Perline Aline Delle; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie & Ystrom, Eivind (2026). How Schools and Neighborhoods Shape the Translation of Polygenic Personality Indices into Academic Outcomes. Full text in Research Archive Show summary

  The Big Five personality traits are robust predictors of individual differences in academic outcomes, yet the mechanisms through which they shape the outcomes remain unclear. Building on our prior work showing contextual moderation of non-cognitive polygenic indices (PGI), we hypothesize that personality traits likewise do not exert uniform influences across contexts. Instead, their effects on academic outcomes emerge through dynamic interactions with the social and economic environments in which individuals develop. Recent GWAS on Big Five personality traits enable the construction of PGIs that quantify the individual-level genetic propensities, and are largely independent of the environment and minimize reverse causality. Using data from ~32,000 trios in the Norwegian Mother, Father, and Child Cohort Study (MoBa) linked to national school and residential registries, we apply multilevel models to investigate how personality-related PGIs contribute to students’ grade point average (GPA), and how these associations vary across latent school and neighborhood contexts. We further test the extent to which the measured socioeconomic status aggregates at the school and neighborhood level interact with individual liability in personality traits. This work aims to provide a comprehensive framework for understanding how individual propensities for personality become developmentally expressed into academic outcomes within real-world contextual ecologies.

• Bjørndal, Ludvig Daae; Valstad, Mathias; Eilertsen, Espen Moen; Ayorech, Ziada; Ofstad, Sverre Berg & Salvatore, Jessica E. [Show all 8 contributors for this article] (2026). Peer effects contribute to psychiatric disorder risk: A population-wide study. Full text in Research Archive
• Sunde, Hans Fredrik; Eilertsen, Espen Moen & Torvik, Fartein Ask (2025). Combining Genetic and Phenotypic Data in Extended Families to Investigate Indirect Assortative Mating and Gene–Environment Correlations. doi: 10.1007/s10519-025-10237-x. Full text in Research Archive Show summary

  Assortative mating and gene-environment correlations complicate the estimation of genetic and environmental effects, yet their impact remains difficult to quantify. We previously developed a theoretical framework for studying indirect assortative mating, which we applied in a new twin model. Here, we apply this framework by updating and expanding the Correlation in Genetic Signal (rGenSi) model. Incor-porating polygenic indices and phenotypic data from extended family pedigrees, the model leverages correlations between partners, relatives and relatives-in-law to investigate (1) the relative importance of social and genetic homogamy, (2) the presence and magnitude of gene-envi-ronment correlations, and (3) the noisiness of the polygenic index—all within a single structural equation model. This approach can help clarify how assortative mating, gene-environment correlations, and the lack of signal each affect polygenic indices, ultimately improving the interpretation of genetic and environmental contributions to complex traits.

• Czajkowski, Nikolai Olavi; Eilertsen, Espen Moen; Valstad, Mathias; Eftedal, Nikolai Haahjem & Ystrøm, Eivind (2025). A Bayesian Framework for Zygosity Classification and Heritability Estimation Using Nationwide Registry Data. Full text in Research Archive
• Porneso, Ralph Pascual Ortiz; Havdahl, Alexandra; Eilertsen, Espen Moen & Ystrøm, Eivind (2025). Genetic Non-Additivity Reveals Variants in Complex Traits. doi: https:/geneforum.ee/wp-content/uploads/2025/09/Gene-Forum-Poster-Abstract-book.pdf. Full text in Research Archive Show summary

  Background: The contribution of non-additive genetic variation in human traits is nil for dominance, small for epistasis and, theory suggests, minimal for gene-environment interaction. Evidence from behavioral genetics indicates genetic interactions play a role in cognitive traits, and recent genome-wide association studies (GWAS) on height and BMI have identified single nucleotide polymorphisms (SNPs) involved in interactions. This study is a first step to uncover the molecular mechanisms behind gene-gene and gene- environment interactions and, in part, bridge the gap in the missing heritability problem. Study question: Are there SNPs associated with complex traits plasticity? Methods: We used a non-linear mixed effects framework to concurrently estimate SNPs’ mean (i.e. additive) and within individual variability (i.e. non-additive) effects on height and BMI at 6, 8 and 12 months (N=~45,000) and Math and Reading scores at grades 5, 8 and 9 (N=~65,000) from the Norwegian Mother Father and Child cohort (MoBa). We compared our models against a newly developed pipeline, trajGWAS, which restricts discovery to variants with linear within subject (WS) variance effects. Our approach relaxes this restriction. In addition, we investigated whether time-varying effects overlap with non- additive effects. Main results: We found putative “plasticity” variants with linear and non-linear effects. We provide within-individual variability summary statistics for height, BMI, Math and Reading. We found SNP time-varying effects explain ~1% of non-additive effects on average but found no overlap. Limitations: At present, our pipeline runs only using multiple cores and takes a considerable amount of compute hours.

• Porneso, Ralph Pascual Ortiz; Havdahl, Alexandra; Eilertsen, Espen Moen & Ystrøm, Eivind (2025). Non-additive genetic effects and complex traits plasticity. Full text in Research Archive Show summary

  Genome-wide association studies (GWAS) on educational attainment and related outcomes have succeeded at identifying hundreds to thousands of genetic variants with small additive effects using measures collected at a single time point. Recently, GWAS leveraging measures collected at multiple time points have found novel genetic associations, suggesting the presence of previously undetected time-specific variants. We hypothesized that a subset of these variants may be involved in gene-by-gene or gene-by-environment interaction. In the present study, we expanded the GWAS framework by estimating genetic effects on the residual variance. We used non-linear mixed effects (NLME) and double generalized linear models (DGLM) to concurrently estimate mean and within individual variance effects on academic performance in Math and Reading at grades 5, 8 and 9 in ~65,000 children from the Norwegian Mother Father and Child cohort (MoBa). We compared our models against a newly developed pipeline, trajGWAS, which restricts variant discovery to those with log-linear within subject (WS) variance effects. Our approach does not impose this restriction and found variants with non-linear variance effect. We replicated findings from other variance-based approaches that non-additive effects co-occur with mean effects. We decorrelated these effects and provide summary statistics for Math and Reading. This study is a first step to better understanding gene-by-gene and gene-by-environment interactions and shed light on the genetic correlates and potential mechanisms involved in complex trait plasticity.

• Eilertsen, Espen Moen; Ayorech, Ziada Ng'ombo Laurel; Cheesman, Rosa Catherine Gillespie & Ystrøm, Eivind (2025). Et mangfold av ulikhet: Fra økonomi til gener. Full text in Research Archive
• Peng, Qiyuan; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Rietveld, Cornelius A. (Niels); Ystrøm, Eivind & Havdahl, Alexandra (2025). Parental Influence on Children's Educational Achievements: Analysing Direct and Indirect Genetic Effects through Trio-GCTA. doi: https:/www.sv.uio.no/psi/english/research/news-and-events/events/conferences/2025/genetics-and-social-sciences-conference--2025.html. Full text in Research Archive
• Porneso, Ralph Pascual Ortiz; Havdahl, Alexandra; Eilertsen, Espen Moen & Ystrøm, Eivind (2025). Genetic non-additivity reveals variants in complex traits plasticity. Full text in Research Archive Show summary

  In human complex traits, the contribution of non-additive relative to additive genetic variation is nil (dominance) to small (genetic interactions) which makes variant discovery difficult to achieve (Hivert, 2018). Even with larger samples, gene-gene and gene-environment interaction studies face several technical challenges (e.g. greater multiple testing burden, collecting and modelling correlated factors, etc) that impede progress in uncovering biological insights behind trait plasticity . We work around these issues by concurrently modelling the effect of single nucleotide polymorphisms (SNPs) on trait level, which shifts the distribution, and variability, which generates heteroscedasticity (unequal variance across genotype levels) resulting in the spreading out of phenotypic values around a mean. This approach does not require explicit interaction terms to be fitted to the data thereby lessening both computational complexity and multiple testing burden encountered by more traditional approaches. We estimate SNP effects on trait level (additive) and variability (non-additive) using a longitudinal heteroscedastic mixed effects model that assume uncorrelated variance components. In total, we found 25 lead putative plasticity SNPs (i.e. 2 for infant length, 11 for BMI, 5 for math and 7 for reading) of which 5 (1 for infant length and 4 for BMI) were previously reported in epistatic or gene-environment interaction in independent studies. We show that non-additive, time-varying and additive effects are correlated with each other across all 4 traits, indicating additive genetic variation captures SNP interaction effects. Our findings provide SNP-based evidence that non-additive genetic variation contributes to complex traits including height.

• Ayorech, Ziada Ng'ombo Laurel; Cheesman, Rosa Catherine Gillespie; Demange, Perline Aline Delle; Eilertsen, Espen Moen; Valstad, Mathias & Ystrøm, Eivind (2025). How the importance of family history and gender for receiving a depression diagnosis varies over GP’s. Full text in Research Archive
• Ayorech, Ziada Ng'ombo Laurel; Cheesman, Rosa Catherine Gillespie; Demange, Perline Aline Delle; Eilertsen, Espen Moen & Ystrøm, Eivind (2025). Leveraging family-based data reveals gene-environment interplay in life course depression. Full text in Research Archive
• Demange, Perline Aline Delle; Eilertsen, Espen Moen & Ystrøm, Eivind (2025). Beyond trio: genetic effects in the entire extended family. Full text in Research Archive
• Demange, Perline Aline Delle; Eilertsen, Espen Moen & Ystrøm, Eivind (2025). Beyond trio: genetic effects in the extended family. Full text in Research Archive
• Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada Ng'ombo Laurel & Ystrøm, Eivind (2024). Parent SES and young people's mental health. Full text in Research Archive
• Cheesman, Rosa Catherine Gillespie; Eilertsen, Espen Moen; Ayorech, Ziada Ng'ombo Laurel; Ystrøm, Eivind; Hootegem, Arno Van & Lyngstad, Torkild Hovde (2024). Parent SES and offspring mental health. Full text in Research Archive
• Ayorech, Ziada Ng'ombo Laurel; Cheesman, Rosa Catherine Gillespie; Demange, Perline Aline Delle; Eilertsen, Espen Moen; Valstad, Mathias & Ystrøm, Eivind (2024). GEOGRAPHICAL STRATIFICATION IN RECEIVING A DEPRESSION DIAGNOSIS IN THE NORWEGIAN POPULATION. doi: https:/www.sciencedirect.com/science/article/abs/pii/S0924977X24005455. Full text in Research Archive Show summary

  Background Depression runs in families, has a striking female preponderance, and in 2030 is predicted to be the leading cause of disease burden worldwide. Receiving a depression diagnosis is critical for access to appropriate treatment to alleviate the debilitating symptoms associated with this common disorder. Evidence that patient characteristics can contribute to who receives a diagnosis is well documented, however the extent to which GP tendencies for diagnosing depression are geographically stratified is unknown, in part due to the sparsity of large scale diagnostic data in population cohorts. Methods Here we capitalize on registry data for ∼ 5 million Norwegian adults including all ICPC2 depression codes, GP, clinic and residential identifiers. Multilevel models are used to test whether the role of familial risk (i.e., affected siblings) in predicting diagnosis varies as a function of geographical location and GP characteristics. In addition we test whether GP diagnosing varies by patients genetic risk and self-report symptoms by adding depression polygenic scores and symptom checklist data for a subset of the population (200,000 genotyped participants in the Norwegian Mother Father and Child study (Moba)) to our models. Results We provide descriptions of depression clusters across the entire Norwegian country and critical insight into the path from symptoms to diagnosis. Crucially, this novel approach informs on whether provider leniency impacts the genetic signal captured in large scale genome-wide association studies of depression. Discussion These results will have implications for academics, clinicians and the more than 300 million individuals and their families suffering from depression worldwide.

• Qin, Qi; Ystrøm, Eivind; Eilertsen, Espen Moen; Ofstad, Sverre Berg; Ayorech, Ziada & Cheesman, Rosa Catherine Gillespie (2024). School-level Moderation of Multiple Within- Family Polygenic Index Effects on Educational Performance in MoBa (n=27476 Trios). Full text in Research Archive
• Sunde, Hans Fredrik; Eftedal, Nikolai Haahjem; Cheesman, Rosa Catherine Gillespie; Corfield, Elizabeth Claire; Kleppestø, Thomas Haarklau & Seierstad, Anne Caroline [Show all 9 contributors for this article] (2024). Genetic similarity between relatives provides evidence on the presence and history of assortative mating. Full text in Research Archive
• Eilertsen, Espen Moen; Eftedal, Nikolai Haahjem; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Ebeltoft, Joakim Coleman & Sunde, Hans Fredrik [Show all 9 contributors for this article] (2024). Multivariate parental effects across the internalizing-externalizing spectrum in childhood: results from the Norwegian Mother, Father, and Child Cohort Study. Full text in Research Archive
• Valstad, Mathias; Eilertsen, Espen Moen; Timpe, Clara Marie Fides; Yang, Tianfang; Eftedal, Nikolai Haahjem & Reichborn-Kjennerud, Ted [Show all 8 contributors for this article] (2024). Genetic and environmental effects on diagnosed Borderline Personality Disorder (BPD) without clinic bias. Full text in Research Archive
• Ebeltoft, Joakim Coleman; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Hootegem, Arno Van & Lyngstad, Torkild Hovde [Show all 7 contributors for this article] (2024). Triangulating Approaches to Evaluate the Genetic and Environmental Composition of Socioeconomic Status. Full text in Research Archive
• Porneso, Ralph Pascual Ortiz; Eilertsen, Espen Moen; Havdahl, Alexandra & Ystrøm, Eivind (2024). Non-additive genetic effects in academic performance. Full text in Research Archive
• Porneso, Ralph Pascual Ortiz; Eilertsen, Espen Moen; Havdahl, Alexandra & Ystrøm, Eivind (2024). Identifying genetic variants with non-additive and time-varying genetic effects using longitudinal data. Full text in Research Archive
• Ystrøm, Eivind; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada & Demange, Perline Aline Delle (2024). The dark matter of parenting – estimating the environmental importance of family members using genetics. Full text in Research Archive
• Cheesman, Rosa Catherine Gillespie; Anapaz, Ville; Alten, Sjoerd van; Abdellaoui, Abdel; Ebeltoft, Joakim Coleman & Porneso, Ralph Pascual Ortiz [Show all 16 contributors for this article] (2024). The Genetics of Educational Fields. Full text in Research Archive
• Peng, Qiyuan; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Rietveld, Cornelius A.; Ystrøm, Eivind & Havdahl, Alexandra (2024). Parental Influence on Children's Educational Achievements: Analyzing Direct and Indirect Genetic Effects through Trio-GCTA. Full text in Research Archive
• Ebeltoft, Joakim Coleman; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Hootegem, Arno Van & Lyngstad, Torkild Hovde [Show all 7 contributors for this article] (2024). Parent SES and young people's mental health: Doctoral project. Full text in Research Archive
• Qin, Qi; Ystrøm, Eivind; Eilertsen, Espen Moen; Ofstad, Sverre Berg; Ayorech, Ziada & Cheesman, Rosa Catherine Gillespie (2024). School-level Moderation of Multiple Within- Family Polygenic Index Effects on Educational Performance in MoBa (n=27476 Trios). Full text in Research Archive
• Sunde, Hans Fredrik; Eilertsen, Espen Moen & Torvik, Fartein Ask (2024). Rethinking indirect assortative mating. Full text in Research Archive
• Eilertsen, Espen Moen; Torvik, Fartein Ask & Sunde, Hans Fredrik (2024). Rethinking partner similarity: Understanding indirect assortative mating and its consequences for educational attainment. Full text in Research Archive
• Valstad, Mathias; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Demange, Perline Aline Delle & Eftedal, Nikolai Haahjem [Show all 8 contributors for this article] (2024). Indirect genetic effects of siblings. Full text in Research Archive
• Demange, Perline Aline Delle; Eilertsen, Espen Moen & Ystrøm, Eivind (2024). Beyond trio: genetic effects in the extended family and proximal environments. Full text in Research Archive
• Peng, Qiyuan; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Rietveld, Cornelius A.; Ystrøm, Eivind & Havdahl, Alexandra (2024). Parental Influence on Children's Educational Achievements: Analyzing Direct and Indirect Genetic Effects through Trio-GCTA. Full text in Research Archive
• Demange, Perline Aline Delle; Eilertsen, Espen Moen & Ystrøm, Eivind (2024). Beyond trio: genetic effects in the extended family and proximal environments. Full text in Research Archive
• Peng, Qiyuan; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Rietveld, Cornelius A.; Ystrøm, Eivind & Havdahl, Alexandra (2024). Parental Influence on Children's Educational Achievements: Analyzing Direct and Indirect Genetic Effects through Trio-GCTA. Full text in Research Archive
• Porneso, Ralph Pascual Ortiz; Eilertsen, Espen Moen; Havdahl, Alexandra & Ystrøm, Eivind (2024). Non-additive genetic effects in academic performance. Full text in Research Archive
• Porneso, Ralph Pascual Ortiz; Eilertsen, Espen Moen; Havdahl, Alexandra & Ystrøm, Eivind (2024). Identifying genetic variants with non-additive and time-varying effects using longitudinal data. Full text in Research Archive
• Hegemann, Laura; Eilertsen, Espen Moen; Pettersen, Johanne Hagen; Corfield, Elizabeth Claire; Cheesman, Rosa Catherine Gillespie & Frach, Leonard [Show all 11 contributors for this article] (2024). Direct and Indirect Genetic Effects on Early Neurodevelopmental Traits (updated results). Full text in Research Archive
• Pettersen, Johanne Hagen; Eilertsen, Espen Moen; Hegemann, Laura; Hannigan, Laurie John; Lund, Ingunn Olea & Jensen, Pia [Show all 12 contributors for this article] (2024). Direct and indirect genetic inluences on mental distress in mother-father-offspring trios during the Covid-19 lockdown. Full text in Research Archive
• Ebeltoft, Joakim Coleman; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Hootegem, Arno Van & Lyngstad, Torkild Hovde [Show all 7 contributors for this article] (2024). Triangulating Approaches to Evaluate the Genetic and Environmental Composition of Socioeconomic Status: Multi-method study. Full text in Research Archive
• Ebeltoft, Joakim Coleman; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Hootegem, Arno Van & Lyngstad, Torkild Hovde [Show all 7 contributors for this article] (2024). Genetic and environmental composition of SES. Full text in Research Archive
• Ebeltoft, Joakim Coleman; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Hootegem, Arno Van & Lyngstad, Torkild Hovde [Show all 7 contributors for this article] (2024). Doctoral project: Socioeconomic status and young people's mental health. Full text in Research Archive
• Eftedal, Nikolai Haahjem; Eilertsen, Espen Moen; Sunde, Hans Fredrik; Kleppestø, Thomas Haarklau; Ystrøm, Eivind & Czajkowski, Nikolai Olavi (2023). Correlations on Norwegian national standardized tests between millions of pairs of relatives: Exploring the impacts of assortative mating and parental effects. Full text in Research Archive
• Ahmadzadeh, Yasmin I.; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ystrøm, Eivind & McAdams, Tom A. (2023). Are mothers’ prenatal emotional symptoms influenced by the foetal genome? Exploring the possibility of child-to- parent effects during pregnancy. Full text in Research Archive
• Sunde, Hans Fredrik; Eftedal, Nikolai Haahjem; Cheesman, Rosa Catherine Gillespie; Corfield, Elizabeth Claire; Kleppestø, Thomas Haarklau & Seierstad, Anne Caroline [Show all 9 contributors for this article] (2023). Genetic similarity between relatives provides evidence on the presence and history of assortative mating. Full text in Research Archive
• Cheesman, Rosa Catherine Gillespie; Eilertsen, Espen Moen & Ystrøm, Eivind (2023). School-level Moderation of Multiple Within- Family Polygenic Index Effects on Educational Performance in MoBa (n=27476 Trios). Full text in Research Archive
• Sunde, Hans Fredrik; Eftedal, Nikolai Haahjem; Cheesman, Rosa Catherine Gillespie; Corfield, Elizabeth Claire; Kleppestø, Thomas Haarklau & Seierstad, Anne Caroline [Show all 9 contributors for this article] (2023). Assortative mating strongly increases genetic similarity between distant relatives. Full text in Research Archive
• Maes, Hermine H.; Eftedal, Nikolai Haahjem; Eilertsen, Espen Moen & Ystrøm, Eivind (2023). Children of Relatives and Parents of Twins Modeling of BMI and Education in MoBa. Full text in Research Archive
• Sunde, Hans Fredrik; Eftedal, Nikolai Haahjem; Cheesman, Rosa Catherine Gillespie; Corfield, Elizabeth Claire; Kleppestø, Thomas Haarklau & Seierstad, Anne Caroline [Show all 9 contributors for this article] (2023). Assortative mating increases genetic similarity among distant relatives: evidence from polygenic scores. Full text in Research Archive
• Sunde, Hans Fredrik; Eilertsen, Espen Moen; Kinge, Jonas Minet; Kleppestø, Thomas Haarklau; Nordmo, Magnus & Caspi, Avshalom [Show all 8 contributors for this article] (2023). Parental income and mental disorders from age 10 to 35: A genetically informative population study. Full text in Research Archive
• Hegemann, Laura; Corfield, Elizabeth Claire; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ask, Helga & Hannigan, Laurie John [Show all 7 contributors for this article] (2023). Indirect and Direct Genetic Effects in Early Neurodevelopmental Traits. Full text in Research Archive
• Torvik, Fartein Ask; Sunde, Hans Fredrik; Cheesman, Rosa Catherine Gillespie; Eftedal, Nikolai Haahjem; Ystrøm, Eivind & Eilertsen, Espen Moen (2023). Within- and cross-trait assortative mating for educational attainment and mental and somatic health conditions: a total population study. Full text in Research Archive
• Ebeltoft, Joakim Coleman; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Ayorech, Ziada; Qin, Qi & Ystrøm, Eivind (2023). The inheritance of inequality: Comparing heritability estimates of socioeconomic status. Full text in Research Archive
• Ayorech, Ziada; Cheesman, Rosa Catherine Gillespie; Eilertsen, Espen Moen; Havdahl, Alexandra & Ystrøm, Eivind (2023). Family-based approaches to gene-environment interplay. Full text in Research Archive
• Cheesman, Rosa Catherine Gillespie; Ystrom, Eivind; Ayorech, Ziada; Eilertsen, Espen Moen; Ystrøm, Eivind & Ayorech, Ziada (2023). The Anatomy of Educational Fields. Full text in Research Archive
• Cheesman, Rosa Catherine Gillespie; Ystrom, Eivind; Eilertsen, Espen Moen; Ayorech, Ziada & Ystrøm, Eivind (2023). The anatomy of educational fields. Full text in Research Archive
• Ayorech, Ziada; Cheesman, Rosa Catherine Gillespie; Eilertsen, Espen Moen; Havdahl, Alexandra & Ystrøm, Eivind (2023). The genetics of depression across the childbearing years. Full text in Research Archive
• Ebeltoft, Joakim; Ystrom, Eivind; Eilertsen, Espen Moen & Ayorech, Ziada (2026). Dissecting intergenerational patterns of socioeconomic status and mental disorders in Norway. Universitetet i Oslo. Full text in Research Archive Show summary

  Socioeconomic status (SES) and mental disorders run in families—representing intergenerational persistence of advantages and disadvantages. Through three original research studies, this thesis investigates intergenerational patterns of socioeconomic status and mental disorders in Norway using genetically informed designs. First, in paper 1, I explore the coarse-grained etiology of the “big four” SES indicators —education, income, occupation, and wealth. By triangulating four advanced genetic methods, I demonstrate common and unique genetic and environmental sources of variance in parent SES. The substantial common variation across the “big four” is linked to genetic and shared environmental influences, while the considerable unique variance is explained by non-shared environment variation. Second, in paper 2, I assess the risk of mental disorders in young people given their parents’ SES—wealth in particular. In multivariable models including the “big four,” parental wealth is the strongest predictor of most mental disorder diagnoses in children, adolescents, and young adults. Significant associations between parent wealth and risk of mental disorders in young people persist after controlling for sibling-shared genetic and environmental factors. Third, in paper 3, I investigate the effects of children’s genetic differences on parents’ economic outcomes from 3 years before birth to 15 years after birth. By controlling for parent genetic factors, child genetic effects were identified using two methods. We found no conclusive evidence of child genetic effects on parent income, wealth, and government transfers. Three broad causal models can explain SES and mental disorder outcome correlations between parents (X) and their children (Y): A) third factors causing correlated observations (X←Z→Y), B) parent factors causing child outcomes (X→Y), and C) child factors causing parent outcomes (X←Y). Paper 1 provides evidence of model A, showing how common genetic and environmental factors explain large shares of the variance between the “big four” SES indicators. Paper 2 provides evidence of both model A and B, indicating that both shared genetic and environmental factors and parental wealth influence mental disorder risk in their children. Paper 3 provides inconclusive evidence of model C child genetic effects on their parents’ economic outcomes. This thesis argues that genetically informed designs are valuable for dissecting at least three important conceptual angles with regard to intergenerational patterns of SES and mental disorders: (i) genetic architecture as the focus—estimating the relative magnitude genetic contributions to phenotypes, and genetic correlations between phenotypes (paper 1); (ii) genetics as a confounder—estimating social effects while accounting for genetic similarity in families (papers 2 and 3), (iii) genetics as a proxy for a social effect—estimating socially-mediated genetic influences on another person’s phenotype (paper 3).

• Peng, Qiyuan; Eilertsen, Espen Moen; Cheesman, Rosa Catherine Gillespie; Rietveld, Cornelius A.; Ystrom, Eivind & Havdahl, Alexandra (2025). Parental Influence on Children’s Educational Achievements: Analysing Direct and Indirect Genetic Effects through Trio-GCTA. bioRxiv. doi: https:/www.biorxiv.org/content/10.64898/2025.12.03.691991v1.article-info. Full text in Research Archive Show summary

  Educational achievement is a key predictor of later-life outcomes, including financial security, social mobility, health, and mortality. Knowing its familial determinants, such as genetic predispositions, is crucial for understanding intergenerational educational mobility and addressing educational inequality. Here, we disentangle direct and indirect genetic effects on educational achievement using trio genome-wide complex trait analysis (Trio-GCTA). Leveraging up to 23,200 genotyped parent–offspring trios from the Norwegian Mother, Father, and Child Cohort Study (MoBa), we find that direct genetic effects explain 15-21% of the variance in educational achievements, including 8th-grade national assessments in Math, Reading, and English, and 10th-grade grade point average (GPA). Notably, indirect genetic effects additionally explain 7-15% of the variance. Both mothers and fathers exert notable influences, exceeding those suggested in previous studies. Moreover, positive gene–environment correlations between parents and offspring show that the intrafamilial environment and children’s genetic predisposition are dependent and mutually reinforcing.

• Hegemann, Laura; Eilertsen, Espen Moen; Pettersen, Johanne Hagen; Corfield, Elizabeth Claire; Cheesman, Rosa Catherine Gillespie & Frach, Leonard [Show all 11 contributors for this article] (2025). Direct and Indirect Genetic Effects on Early Neurodevelopmental Traits (preprint). MedRxiv. Full text in Research Archive

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