Abstract
Offspring resemble their parents for both genetic and environmental reasons. Understanding the relative magnitude of these alternatives has long been a core interest in behavioral genetics research, but traditional designs, which compare phenotypic covariances to make inferences about unmeasured genetic and environmental factors, have struggled to disentangle them. Recently, Kong et al. (2018) showed that by correlating offspring phenotypic values with the measured polygenic score of parents’ nontransmitted alleles, one can estimate the effect of “genetic nurture”—a type of passive gene–environment covariation that arises when heritable parental traits directly influence offspring traits. Here, we instantiate this basic idea in a set of causal models that provide novel insights into the estimation of parental influences on offspring. Most importantly, we show how jointly modeling the parental polygenic scores and the offspring phenotypes can provide an unbiased estimate of the variation attributable to the environmental influence of parents on offspring, even when the polygenic score accounts for a small fraction of trait heritability. This model can be further extended to (a) account for the influence of different types of assortative mating, (b) estimate the total variation due to additive genetic effects and their covariance with the familial environment (i.e., the full genetic nurture effect), and (c) model situations where a parental trait influences a different offspring trait. By utilizing structural equation modeling techniques developed for extended twin family designs, our approach provides a general framework for modeling polygenic scores in family studies and allows for various model extensions that can be used to answer old questions about familial influences in new ways.
Highlights
Parents share half of their additive genetic effects with their children, causing resemblance between parent and offspring for heritable traits
Using techniques developed for extended twin family designs, we demonstrate how both disequilibrium and equilibrium assortative mating (AM) can be tested and accounted for in causal models
We show that when the assumption of no AM is met, this model provides a full estimate of VF, regardless of the amount of variance explained by the Polygenic score (PGS) ( 2 )
Summary
Parents share half of their (autosomal) additive genetic effects with their children, causing resemblance between parent and offspring for heritable traits. As noted by Kong et al, T − NT = is an estimate of the direct genetic effect of the PGS, controlling for genetic nurture This model assumes that parameters have reached equilibrium, which implies that variances and covariances are the same across parental and offspring generations. This bivariate model would estimate two direct and two cross-trait VT paths and four genetic nurture paths all while accounting for direct genetic effects, pleiotropy, and AM within and between traits While this may sound like a lot to ask of a model, there is a tremendous amount of unique information contained in the 14-by-14 observed variance-covariance matrix, making this approach powerful if the PGS r2 ’s for both traits are nontrivial. Alternative mechanisms of AM can be formally tested using the rich information available from parent and offspring PGS’s and phenotypes, and when called for, models can be modified to incorporate alternative mechanisms of AM
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