Abstract

Research on environmental and genetic pathways to complex traits such as educational attainment (EA) is confounded by uncertainty over whether correlations reflect effects of transmitted parental genes, causal family environments, or some, possibly interactive, mixture of both. Thus, an aggregate of thousands of alleles associated with EA (a polygenic risk score; PRS) may tap parental behaviors and home environments promoting EA in the offspring. New methods for unpicking and determining these causal pathways are required. Here, we utilize the fact that parents pass, at random, 50% of their genome to a given offspring to create independent scores for the transmitted alleles (conventional EA PRS) and a parental score based on alleles not transmitted to the offspring (EA VP_PRS). The formal effect of non-transmitted alleles on offspring attainment was tested in 2,333 genotyped twins for whom high-quality measures of EA, assessed at age 17 years, were available, and whose parents were also genotyped. Four key findings were observed. First, the EA PRS and EA VP_PRS were empirically independent, validating the virtual-parent design. Second, in this family-based design, children's own EA PRS significantly predicted their EA (β = 0.15), ruling out stratification confounds as a cause of the association of attainment with the EA PRS. Third, parental EA PRS predicted the SES environment parents provided to offspring (β = 0.20), and parental SES and offspring EA were significantly associated (β = 0.33). This would suggest that the EA PRS is at least as strongly linked to social competence as it is to EA, leading to higher attained SES in parents and, therefore, a higher experienced SES for children. In a full structural equation model taking account of family genetic relatedness across multiple siblings the non-transmitted allele effects were estimated at similar values; but, in this more complex model, confidence intervals included zero. A test using the forthcoming EA3 PRS may clarify this outcome. The virtual-parent method may be applied to clarify causality in other phenotypes where observational evidence suggests parenting may moderate expression of other outcomes, for instance in psychiatry.

Highlights

  • Correlations between parenting and outcomes such as offspring educational attainment (EA) are ubiquitous

  • EA is, highly heritable creating a large non-independence in attainment nested within families, χ2(1) = 242.69, p < .0001, ICC = 0.57, so family ID and zygosity were entered as random variables in all models

  • We tested the core hypothesis in a structural equation model, where we were able to model the full nesting within families via a multigroup approach, and include genetic associations among twins and siblings

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Summary

Introduction

Correlations between parenting and outcomes such as offspring EA are ubiquitous. as parents transmit genes and create environments for offspring (Neale & Cardon, 1992), these correlations are confounded. The study found that direct literacy training (such as phonics) did independently predict acquired reading skill, but was unrelated to maternal language ability This example exemplifies both the possibility of intervention and the risks of confounding leading to incorrect research conclusions. It indicates that effects on child outcomes may reach beyond genetic transmission from parents to include factors such as literacy training These are not direct consequences of parental ability, but are instead factors under at least partial parental control and involve constructing niches for children that include such effective interventions. In this way, they reflect effective parenting competence. This competence may both play an important causal role and itself be heritable

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