Polygenic Scores For Educational Attainment Research Articles

A polygenic score for educational attainment partially predicts voter turnout

Twin and adoption studies have shown that individual differences in political participation can be explained, in part, by genetic variation. However, these research designs cannot identify which genes are related to voting or the pathways through which they exert influence, and their conclusions rely on possibly restrictive assumptions. In this study, we use three different US samples and a Swedish sample to test whether genes that have been identified as associated with educational attainment, one of the strongest correlates of political participation, predict self-reported and validated voter turnout. We find that a polygenic score capturing individuals' genetic propensity to acquire education is significantly related to turnout. The strongest associations we observe are in second-order midterm elections in the United States and European Parliament elections in Sweden, which tend to be viewed as less important by voters, parties, and the media and thus present a more information-poor electoral environment for citizens to navigate. A within-family analysis suggests that individuals' education-linked genes directly affect their voting behavior, but, for second-order elections, it also reveals evidence of genetic nurture. Finally, a mediation analysis suggests that educational attainment and cognitive ability combine to account for between 41% and 63% of the relationship between the genetic propensity to acquire education and voter turnout.

Genetic Risk for Smoking: Disentangling Interplay Between Genes and Socioeconomic Status

This study aims to disentangle the contribution of genetic liability, educational attainment (EA), and their overlap and interaction in lifetime smoking. We conducted genome-wide association studies (GWASs) in UK Biobank (N = 394,718) to (i) capture variants for lifetime smoking, (ii) variants for EA, and (iii) variants that contribute to lifetime smoking independently from EA (‘smoking-without-EA’). Based on the GWASs, three polygenic scores (PGSs) were created for individuals from the Netherlands Twin Register (NTR, N = 17,805) and the Netherlands Mental Health Survey and Incidence Study-2 (NEMESIS-2, N = 3090). We tested gene–environment (G × E) interactions between each PGS, neighborhood socioeconomic status (SES) and EA on lifetime smoking. To assess if the PGS effects were specific to smoking or had broader implications, we repeated the analyses with measures of mental health. After subtracting EA effects from the smoking GWAS, the SNP-based heritability decreased from 9.2 to 7.2%. The genetic correlation between smoking and SES characteristics was reduced, whereas overlap with smoking traits was less affected by subtracting EA. The PGSs for smoking, EA, and smoking-without-EA all predicted smoking. For mental health, only the PGS for EA was a reliable predictor. There were suggestions for G × E for some relationships, but there were no clear patterns per PGS type. This study showed that the genetic architecture of smoking has an EA component in addition to other, possibly more direct components. PGSs based on EA and smoking-without-EA had distinct predictive profiles. This study shows how disentangling different models of genetic liability and interplay can contribute to our understanding of the etiology of smoking.

Genetic effects on educational attainment in Hungary.

IntroductionEducational attainment is a substantially heritable trait, and it has recently been linked to specific genetic variants by genome‐wide association studies (GWASs). However, the effects of such genetic variants are expected to vary across environments, including countries and historical eras.MethodsWe used polygenic scores (PGSs) to assess molecular genetic effects on educational attainment in Hungary, a country in the Central Eastern European region where behavioral genetic studies are in general scarce and molecular genetic studies of educational attainment have not been previously published.ResultsWe found that the PGS is significantly associated with the attainment of a college degree as well as the number of years in education in a sample of Hungarian study participants (N = 829). PGS effect sizes were not significantly different when compared to an English (N = 976) comparison sample with identical measurement protocols. In line with previous Estonian findings, we found higher PGS effect sizes in Hungarian, but not in English participants who attended higher education after the fall of Communism, although we lacked statistical power for this effect to reach significance.DiscussionOur results provide evidence that polygenic scores for educational attainment have predictive value in culturally diverse European populations.

The association between polygenic scores for attention-deficit/hyperactivity disorder and school performance: The role of attention-deficit/hyperactivity disorder symptoms, polygenic scores for educational attainment, and shared familial factors.

Polygenic scores (PGS) for attention-deficit/hyperactivity disorder (ADHD) negatively predicts educational attainment (EA), but it remains unclear how ADHD symptoms, PGS for EA, and shared familiar factors influence the associations between PGS for ADHD and school performance. We combined survey data on ADHD symptoms, PGS, and register-based, objective measures of compulsory school performance at age 16 for 6049 twins in the Child and Adolescent Twin Study in Sweden. Linear and instrumental variable (IV) regression models were used to estimate the association between PGS for ADHD and grade point average (GPA), overall and by natural science, humanities, and practically oriented (e.g., sports, arts, music) subject categories. The models were adjusted for parent-rated ADHD symptoms, PGS for EA, and shared familial factors (dizygotic twin comparisons) to examine how these factors influenced the associations between PGS for ADHD and school performance. PGS for ADHD were negatively associated with school performance; β=-0.12, 95% confidence interval = (-0.15, -0.09) for overall GPA with minor differences by subject category. Adjustment for ADHD symptoms attenuated these associations to a small degree compared to PGS for EA, and shared familial factors respectively. Stronger associations were observed using IV regressions compared to linear regression. However, in the IV regression analyses, most associations between PGS for ADHD and GPA in the practically oriented subject category were not significant. Associations between PGS for ADHD and school performance are to a small degree influenced by ADHD symptoms, compared to PGS for EA and shared familial factors. These results highlight important considerations for research using PGS for ADHD to control for genetic factors, and for future clinical applications aiming to determine genetic liability towards ADHD.

Educational attainment polygenic score predicts inhibitory control and academic skills in early and middle childhood.

Inhibitory control skills are important for academic outcomes across childhood, but it is unknown whether inhibitory control is implicated in the association between genetic variation and academic performance. This study examined the relationship between a GWAS-based (EduYears) polygenic score indexing educational attainment (EA PGS) and inhibitory control in early (Mage =3.80 years) and middle childhood (Mage =9.18 years), and whether inhibitory control in early childhood mediated the relation between EA PGS and academic skills. The sample comprised 731 low-income and racially/ethnically diverse children and their families from the longitudinal early steps multisite study. EA PGS predicted middle childhood inhibitory control (estimate=0.09, SE=0.05, p < 0.05) and academic skills (estimate=0.18, SE=0.05, p < 0.01) but did not predict early childhood inhibitory control (estimate=0.08, SE=0.05, p=0.11); thus, mediation was not tested. Sensitivity analyses showed that effect sizes were similar across European and African American groups. This study suggests that inhibitory control could serve as a potential mechanism linking genetic differences to educational outcomes.

Pygmalion in the genes? On the potentially negative impacts of polygenic scores for educational attainment

Polygenic scores for educational attainment and related variables, such as IQ and “mathematical ability” are now readily available via direct-to-consumer genetic testing companies. Some researchers are even proposing the use of genetic tests in educational settings via “precision education,” in which individualized student education plans would be tailored to polygenic scores. The potential psychosocial impacts of polygenic scores for traits and outcomes relevant to education, however, have not been assessed. In online experiments, we asked participants to imagine hypothetical situations in which they or their classmates had recently received polygenic scores for educational attainment. Participants prompted to answer multi-choice questions as though they had received their own low-percentile score, compared to a control condition, scored significantly lower on measures of self-esteem and of self-perceived competence, academic efficacy, and educational potential. Similarly, those asked to evaluate a hypothetical classmate as though the classmate had received a low-percentile score attributed significantly lower academic efficacy and educational potential, compared to a control condition. Through possible mechanisms of stigma and self-fulfilling prophecies, our results highlight the potential psychosocial harms of exposure to low-percentile polygenic scores for educational attainment.

Evidence for the Scarr-Rowe Effect on Genetic Expressivity in the Health and Retirement Study.

The Scarr-Rowe effect is a gene × environment interaction, which is characterized by a negative association between exposure to low socioeconomic status (SES) environments and the additive heritability of cognitive ability. Utilizing a polygenic score for educational attainment (EA3), it was found that the two-way interaction between EA3 and parental educational attainment (EA; used as a proxy for parental SES) was a significant positive predictor of participants' composite cognitive ability (IQ) score (β = .018, SE = .008, p = .028) after controlling hierarchically for the direct effects of (population-stratification-controlled) EA3, parental EA, and 20 distinct interaction terms (10 involving the interactions between the principal components [PCs] and EA3, and 10 involving the interaction between the PCs and parental EA). The presence of this interaction is consistent with the Scarr-Rowe effect, as the expressivity of EA3 on cognitive ability increases with increasing parental EA. No statistically significant sex differences in the effect magnitudes were found, although the effect was significantly present in the female but not male sample.

Using multivariate endophenotypes to identify psychophysiological mechanisms associated with polygenic scores for substance use, schizophrenia, and education attainment.

Background.To better characterize brain-based mechanisms of polygenic liability for psychopathology and psychological traits, we extended our previous report (Liu et al. Psychophysiological endophenotypes to characterize mechanisms of known schizophrenia genetic loci. Psychological Medicine, 2017), focused solely on schizophrenia, to test the association between multivariate psychophysiological candidate endophenotypes (including novel measures of θ/δ oscillatory activity) and a range of polygenic scores (PGSs), namely alcohol/cannabis/nicotine use, an updated schizophrenia PGS (containing 52 more genome-wide significant loci than the PGS used in our previous report) and educational attainment.Method.A large community-based twin/family sample (N = 4893) was genome-wide genotyped and imputed. PGSs were constructed for alcohol use, regular smoking initiation, lifetime cannabis use, schizophrenia, and educational attainment. Eleven endophenotypes were assessed: visual oddball task event-related electroencephalogram (EEG) measures (target-related parietal P3 amplitude, frontal θ, and parietal δ energy/inter-trial phase clustering), band-limited resting-state EEG power, antisaccade error rate. Principal component analysis exploited covariation among endophenotypes to extract a smaller number of meaningful dimensions/components for statistical analysis.Results.Endophenotypes were heritable. PGSs showed expected intercorrelations (e.g. schizophrenia PGS correlated positively with alcohol/nicotine/cannabis PGSs). Schizophrenia PGS was negatively associated with an event-related P3/δ component [β = −0.032, nonparametric bootstrap 95% confidence interval (CI) −0.059 to −0.003]. A prefrontal control component (event-related θ/antisaccade errors) was negatively associated with alcohol (β = −0.034, 95% CI −0.063 to −0.006) and regular smoking PGSs (β = −0.032, 95% CI −0.061 to −0.005) and positively associated with educational attainment PGS (β = 0.031, 95% CI 0.003–0.058).Conclusions.Evidence suggests that multivariate endophenotypes of decision-making (P3/δ) and cognitive/attentional control (θ/antisaccade error) relate to alcohol/nicotine, schizophrenia, and educational attainment PGSs and represent promising targets for future research.

No support for the hereditarian hypothesis of the Black-White achievement gap using polygenic scores and tests for divergent selection.

Debate about the cause of IQ score gaps between Black and White populations has persisted within genetics, anthropology, and psychology. Recently, authors claimed polygenic scores provide evidence that a significant portion of differences in cognitive performance between Black and White populations are caused by genetic differences due to natural selection, the "hereditarian hypothesis." This study aims to show conceptual and methodological flaws of past studies supporting the hereditarian hypothesis. Polygenic scores for educational attainment were constructed for African and European samples of the 1000 Genomes Project. Evidence for selection was evaluated using an excess variance test. Education associated variants were further evaluated for signals of selection by testing for excess genetic differentiation (Fst ). Expected mean difference in IQ for populations was calculated under a neutral evolutionary scenario and contrasted to hereditarian claims. Tests for selection using polygenic scores failed to find evidence of natural selection when the less biased within-family GWAS effect sizes were used. Tests for selection using Fst values did not find evidence of natural selection. Expected mean difference in IQ was substantially smaller than postulated by hereditarians, even under unrealistic assumptions that overestimate genetic contribution. Given these results, hereditarian claims are not supported in the least. Cognitive performance does not appear to have been under diversifying selection in Europeans and Africans. In the absence of diversifying selection, the best case estimate for genetic contributions to group differences in cognitive performance is substantially smaller than hereditarians claim and is consistent with genetic differences contributing little to the Black-White gap.

Genetic influences on the interactionist model of socioeconomic development: Incorporating polygenic scores for educational attainment into developmental research using the Family Transitions Project (FTP).

Genetic and environmental factors account for variability in a range of developmental outcomes, including socioeconomic status (SES). The challenge is to find ways to incorporate genetic information based on studies using biologically related family members (i.e., studies not involving twins). To address this issue, we computed polygenic scores associated with educational attainment (Lee et al., 2018) for the Family Transitions Project (e.g., R. D. Conger & Conger, 2002) and incorporated them into the model tested by R. D. Conger, Martin, and Masarik, (2021). Polygenic scores correlated with observed educational attainment for all relevant members of the Family Transitions Project. Moreover, polygenic scores were correlated with many of the other constructs in the R. D. Conger et al. (2021) model, pointing to the relevance of genetic factors for process models of SES attainment. At the same time, the primary pathways described by R. D. Conger et al. (2021) remained viable when polygenic scores were included in the analyses, suggesting that the environmental pathways predicted by the interactionist model (e.g., R. D. Conger, Conger, & Martin, 2010) are still tenable. The current study thereby illustrates how genetic information can be included in tests of developmental models to clarify SES attainment across generations. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

The relational genomics of cognitive function: A longitudinal study.

Research in social genetics indicates a person's genome may influence outcomes of those in close relationships. Implications for cognitive function remain unexplored. The current study examined such "metagenomic" patterns among older U.S. couples. Data were from married or cohabiting couples in the 2006-2016 waves of the Health and Retirement Study, nationally representative of U.S. adults over 50. Measures included cognitive function as well as separate polygenic scores for cognition and for educational attainment. Analysis was through parallel process latent growth models. Consistent with a recent "genetic externalities" conception, one partner's polygenic score for educational attainment was linked to the other's baseline levels of cognitive function. Contrary to relational moderation speculations, neither a partner's genetic scores nor educational attainment altered individual-level genetic influences. Findings add to the growing evidence that transpersonal genetic influences in one's proximal context have substantively important implications. Research is needed on the role of non-partnership ties in channeling such effects. Implications for life course theory are discussed.

More Research Needed: There is a Robust Causal vs. Confounding Problem for Intelligence-associated Polygenic Scores in Context to Admixed American Populations

Amongst admixed American populations, polygenic scores for educational attainment and intelligence (eduPGS), genetic ancestry, and cognitive ability covary. We argue that this plausibly could be due to either confounding or to causally-relevant genetic differences between ancestral groups. It is important to determine which scenario is the case in order to better assess the validity of eduPGS. We investigate the robustness of the confounding vs. causal concern by examining, in detail, the relation between eduPGS, ancestry, and general cognitive ability in East Coast Hispanic and non-Hispanic samples. EduPGS predicted g among Hispanics (B = 0.175, N = 506) and all other groups (European: B = 0.230, N = 4914; European-African: B = 0.215, N = 228; African: B = 0.126, N = 2179) with controls for ancestry. Path analyses revealed that eduPGS, but not skin color, partially statistically explained the association between g and European ancestry among both Hispanics and the combined sample. Also, we were unable to account for eduPGS differences between the main ancestral populations using common tests for ascertainment bias and confounding related to population stratification. Overall, our results suggest that eduPGS derived from European samples can be used to predict g in American populations. However, owing to the uncertain cause of the ancestry-related differences in eduPGS, it is not yet clear how the effect of ancestry should be handled. We argue that causally-informative research is needed to determine the source of the relation between eduPGS, genetic ancestry, and cognitive ability. Keywords: Education, Intelligence, Polygenic scores, Hispanics, African-Americans, Philadelphia

Cognitive and brain development is independently influenced by socioeconomic status and polygenic scores for educational attainment.

Genetic factors and socioeconomic status (SES) inequalities play a large role in educational attainment, and both have been associated with variations in brain structure and cognition. However, genetics and SES are correlated, and no prior study has assessed their neural associations independently. Here we used a polygenic score for educational attainment (EduYears-PGS), as well as SES, in a longitudinal study of 551 adolescents to tease apart genetic and environmental associations with brain development and cognition. Subjects received a structural MRI scan at ages 14 and 19. At both time points, they performed three working memory (WM) tasks. SES and EduYears-PGS were correlated (r = 0.27) and had both common and independent associations with brain structure and cognition. Specifically, lower SES was related to less total cortical surface area and lower WM. EduYears-PGS was also related to total cortical surface area, but in addition had a regional association with surface area in the right parietal lobe, a region related to nonverbal cognitive functions, including mathematics, spatial cognition, and WM. SES, but not EduYears-PGS, was related to a change in total cortical surface area from age 14 to 19. This study demonstrates a regional association of EduYears-PGS and the independent prediction of SES with cognitive function and brain development. It suggests that the SES inequalities, in particular parental education, are related to global aspects of cortical development, and exert a persistent influence on brain development during adolescence.

Genetic Associations Between Childhood Psychopathology and Adult Depression and Associated Traits in 42 998 Individuals

Adult mood disorders are often preceded by behavioral and emotional problems in childhood. It is yet unclear what explains the associations between childhood psychopathology and adult traits. To investigate whether genetic risk for adult mood disorders and associated traits is associated with childhood disorders. This meta-analysis examined data from 7 ongoing longitudinal birth and childhood cohorts from the UK, the Netherlands, Sweden, Norway, and Finland. Starting points of data collection ranged from July 1985 to April 2002. Participants were repeatedly assessed for childhood psychopathology from ages 6 to 17 years. Data analysis occurred from September 2017 to May 2019. Individual polygenic scores (PGS) were constructed in children based on genome-wide association studies of adult major depression, bipolar disorder, subjective well-being, neuroticism, insomnia, educational attainment, and body mass index (BMI). Regression meta-analyses were used to test associations between PGS and attention-deficit/hyperactivity disorder (ADHD) symptoms and internalizing and social problems measured repeatedly across childhood and adolescence and whether these associations depended on childhood phenotype, age, and rater. The sample included 42 998 participants aged 6 to 17 years. Male participants varied from 43.0% (1040 of 2417 participants) to 53.1% (2434 of 4583 participants) by age and across all cohorts. The PGS of adult major depression, neuroticism, BMI, and insomnia were positively associated with childhood psychopathology (β estimate range, 0.023-0.042 [95% CI, 0.017-0.049]), while associations with PGS of subjective well-being and educational attainment were negative (β, -0.026 to -0.046 [95% CI, -0.020 to -0.057]). There was no moderation of age, type of childhood phenotype, or rater with the associations. The exceptions were stronger associations between educational attainment PGS and ADHD compared with internalizing problems (Δβ, 0.0561 [Δ95% CI, 0.0318-0.0804]; ΔSE, 0.0124) and social problems (Δβ, 0.0528 [Δ95% CI, 0.0282-0.0775]; ΔSE, 0.0126), and between BMI PGS and ADHD and social problems (Δβ, -0.0001 [Δ95% CI, -0.0102 to 0.0100]; ΔSE, 0.0052), compared with internalizing problems (Δβ, -0.0310 [Δ95% CI, -0.0456 to -0.0164]; ΔSE, 0.0074). Furthermore, the association between educational attainment PGS and ADHD increased with age (Δβ, -0.0032 [Δ 95% CI, -0.0048 to -0.0017]; ΔSE, 0.0008). Results from this study suggest the existence of a set of genetic factors influencing a range of traits across the life span with stable associations present throughout childhood. Knowledge of underlying mechanisms may affect treatment and long-term outcomes of individuals with psychopathology.

Educational attainment polygenic scores are associated with cortical total surface area and regions important for language and memory

It is well established that higher cognitive ability is associated with larger brain size. However, individual variation in intelligence exists despite brain size and recent studies have shown that a simple unifactorial view of the neurobiology underpinning cognitive ability is probably unrealistic. Educational attainment (EA) is often used as a proxy for cognitive ability since it is easily measured, resulting in large sample sizes and, consequently, sufficient statistical power to detect small associations. This study investigates the association between three global (total surface area (TSA), intra-cranial volume (ICV) and average cortical thickness) and 34 regional cortical measures with educational attainment using a polygenic scoring (PGS) approach. Analyses were conducted on two independent target samples of young twin adults with neuroimaging data, from Australia (N ​= ​1097) and the USA (N ​= ​723), and found that higher EA-PGS were significantly associated with larger global brain size measures, ICV and TSA (R2 ​= ​0.006 and 0.016 respectively, p ​< ​0.001) but not average thickness. At the regional level, we identified seven cortical regions—in the frontal and temporal lobes—that showed variation in surface area and average cortical thickness over-and-above the global effect. These regions have been robustly implicated in language, memory, visual recognition and cognitive processing. Additionally, we demonstrate that these identified brain regions partly mediate the association between EA-PGS and cognitive test performance. Altogether, these findings advance our understanding of the neurobiology that underpins educational attainment and cognitive ability, providing focus points for future research.

An Investigation of Psychosis Subgroups With Prognostic Validation and Exploration of Genetic Underpinnings

Identifying psychosis subgroups could improve clinical and research precision. Research has focused on symptom subgroups, but there is a need to consider a broader clinical spectrum, disentangle illness trajectories, and investigate genetic associations. To detect psychosis subgroups using data-driven methods and examine their illness courses over 1.5 years and polygenic scores for schizophrenia, bipolar disorder, major depression disorder, and educational achievement. This ongoing multisite, naturalistic, longitudinal (6-month intervals) cohort study began in January 2012 across 18 sites. Data from a referred sample of 1223 individuals (765 in the discovery sample and 458 in the validation sample) with DSM-IV diagnoses of schizophrenia, bipolar affective disorder (I/II), schizoaffective disorder, schizophreniform disorder, and brief psychotic disorder were collected from secondary and tertiary care sites. Discovery data were extracted in September 2016 and analyzed from November 2016 to January 2018, and prospective validation data were extracted in October 2018 and analyzed from January to May 2019. A clinical battery of 188 variables measuring demographic characteristics, clinical history, symptoms, functioning, and cognition was decomposed using nonnegative matrix factorization clustering. Subtype-specific illness courses were compared with mixed models and polygenic scores with analysis of covariance. Supervised learning was used to replicate results in validation data with the most reliably discriminative 45 variables. Of the 765 individuals in the discovery sample, 341 (44.6%) were women, and the mean (SD) age was 42.7 (12.9) years. Five subgroups were found and labeled as affective psychosis (n = 252), suicidal psychosis (n = 44), depressive psychosis (n = 131), high-functioning psychosis (n = 252), and severe psychosis (n = 86). Illness courses with significant quadratic interaction terms were found for psychosis symptoms (R2 = 0.41; 95% CI, 0.38-0.44), depression symptoms (R2 = 0.28; 95% CI, 0.25-0.32), global functioning (R2 = 0.16; 95% CI, 0.14-0.20), and quality of life (R2 = 0.20; 95% CI, 0.17-0.23). The depressive and severe psychosis subgroups exhibited the lowest functioning and quadratic illness courses with partial recovery followed by reoccurrence of severe illness. Differences were found for educational attainment polygenic scores (mean [SD] partial η2 = 0.014 [0.003]) but not for diagnostic polygenic risk. Results were largely replicated in the validation cohort. Psychosis subgroups were detected with distinctive clinical signatures and illness courses and specificity for a nondiagnostic genetic marker. New data-driven clinical approaches are important for future psychosis taxonomies. The findings suggest a need to consider short-term to medium-term service provision to restore functioning in patients stratified into the depressive and severe psychosis subgroups.

Intergenerational Transmission of Education and ADHD: Effects of Parental Genotypes

It remains a challenge to determine whether children resemble their parents due to nature, nurture, or a mixture of both. Here we used a design that exploits the distinction between transmitted and non-transmitted alleles in genetic transmission from parent to offspring. Two separate polygenic scores (PGS) were calculated on the basis of the transmitted and non-transmitted alleles. The effect of the non-transmitted PGS is necessarily mediated by parental phenotypes, insofar as they contribute to the rearing environment of the offspring (genetic nurturing). We calculated transmitted and non-transmitted PGSs associated with adult educational attainment (EA) and PGSs associated with childhood ADHD in a general population sample of trios, i.e. child or adult offspring and their parents (N = 1120–2518). We tested if the EA and ADHD (non-)transmitted PGSs were associated with childhood academic achievement and ADHD in offspring. Based on the earlier findings for shared environment, we hypothesized to find genetic nurturing for academic achievement, but not for ADHD. In adults, both transmitted (R2 = 7.6%) and non-transmitted (R2 = 1.7%) EA PGSs were associated with offspring EA, evidencing genetic nurturing. In children around age 12, academic achievement was associated with the transmitted EA PGSs (R2 = 5.7%), but we found no support for genetic nurturing (R2 ~ 0.1%). The ADHD PGSs were not significantly associated with academic achievement (R2 ~ 0.6%). ADHD symptoms in children were only associated with transmitted EA PGSs and ADHD PGSs (R2 = 1–2%). Based on these results, we conclude that the associations between parent characteristics and offspring outcomes in childhood are mainly to be attributable to the effects of genes that are shared by parents and children.

Sibling Correlation in Educational Attainment: A Test of Genetic Nurture

The educational attainment of siblings is highly correlated. We test for a specific type of peer effect between siblings in educational attainment: genetic nurture. Specifically, we test whether a person’s educational attainment is correlated with their sibling’s polygenic score (PGS) for educational attainment, controlling for their own PGS for educational attainment. Models estimated using genetic data in the National Longitudinal Survey of Adolescent to Adult Health (Add Health) yield strong evidence of such genetic nurture between siblings, and this result is robust to alternative measures of educational attainment and different measures of polygenic score. Institutional subscribers to the NBER working paper series, and residents of developing countries may download this paper without additional charge at www.nber.org.

Child-Driven Parenting: Differential Early Childhood Investment by Offspring Genotype

A growing literature points to children’s influence on parents’ behavior, including parental investments in children. Further, previous research has shown differential parental response by socioeconomic status to children's birth weight, cognitive ability, and school outcomes – all early life predictors of later socioeconomic success. This study considers an even earlier, more exogenous predictor of parental investments: offspring genotype. Specifically, we analyze (1) whether children’s genetic propensity towards educational success affects parenting during early childhood; and (2) whether parenting in response to children’s genetic propensity towards educational success is socially stratified. Using data from the Avon Longitudinal Survey of Parents and Children (N=7,738), we construct polygenic scores for educational attainment and regress cognitively stimulating parenting behavior during early childhood on these polygenic scores. We use a range of modeling strategies to address the concern that child’s genotype may be proxying unmeasured parent characteristics. Results show that parents provide more cognitive stimulation to children with higher education polygenic scores. This pattern varies by socioeconomic status with college-educated parents responding less to children’s genetic propensity towards educational success than non-college-educated parents do.

Family Disadvantage, Gender and the Returns to Genetic Human Capital

This paper relies on a large-scale sample of genotyped individuals linked with detailed register data in Denmark to investigate the context-dependence of genetic influences on human capital formation. We show that the returns to genetic endowments, measured by a polygenic score for educational attainment, are significantly attenuated by childhood disadvantage. We replicate the findings in a within-family analysis, where we exploit exogenous genetic variation across siblings to control for unobserved family influences. We also explore gender differences in the context-dependence of genetic influences and find the attenuation effect of childhood disadvantage on educational attainment to be significantly stronger for males than for females. We show our findings extend to a representative sample of the Danish population. Our results highlight an important mechanism driving the persistence of disadvantage across generations. We show that children who experience childhood disadvantage are not able to fully realize their educational potential, even in the context of the generous Danish welfare-state.