Oginni, Olakunle, and Sophie von Stumm. 2022. “Do Children Cause the Cognitive Stimulation They Receive? Modelling the Direction of Causality.” PsyArXiv. October 8. psyarxiv.com/pqf78
Abstract
We tested the directionality of associations between children’s early-life cognitive development and the cognitive stimulation that they received from their parents. Our sample included up to 15,314 children from the Twins Early Development Study (TEDS), who were born between 1994 and 1996 and assessed at age 3 and 4 years on cognitive development and cognitive stimulation, including singing rhymes, reading books, and playing games.
Across a series of genetically informative models, we found consistent, bidirectional causal influences from cognitive development at age 3 to cognitive stimulation at age 4, and from cognitive stimulation at age 3 to cognitive development at age 4. The prospective causal paths in both directions accounted for a third and up to half of the constructs’ phenotypic correlations. Our findings emphasize the active role that children play in constructing their learning experiences, and challenge the idea that children are passive recipients of environmental inputs.
Discussion
Twin studies can be used to
strengthen causal inferences for observed associations between two
constructs by controlling for their shared genetic and environmental
influences (McAdams et al., 2021). Specifically, twin studies can
address whether associations between a putatively environmental
exposure and developmental differences in a phenotype remain
significant after accounting for the confounding effects of shared
etiology (i.e., common causes; McAdams et al., 2021). Recent years
have seen an explosion of novel modelling approaches that extend the
classical twin design, which enable causal inferences but are yet to
be systematically applied in psychological research (Eberli et al.,
2019; McAdams et al., 2021). Here, we fitted direction-of-causality
(DoC) models (Heath, 1993), Mendelian Randomization (MR) extensions
of the DoC model (Minică et al., 2018), and cross-lagged twin models
(Burt et al., 2005) to investigate if children’s cognitive
stimulation causes their cognitive development or vice versa at age 3
and 4 years.
We found prospective causal
associations between children’s cognitive development and their
cognitive stimulation that were bidirectional. Thus, contemporaneous
mechanisms drive the causal influences between cognitive ability and
stimulation: Children benefit from experiencing cognitively
stimulating environments, and at the same time their cognitive
development evokes the cognitive stimulation that their parents
provide. Our findings align with a growing body of evidence
documenting that children are not passive recipients of environmental
inputs but select, modify, and create experiences that are correlated
with their genetic proclivities (Bronfenbrenner & Morris, 2006;
Wertz et al., 2019).
The prospective, bidirectional
causal influences between cognitive development and cognitive
stimulation were significant, accounting for between a third to
nearly half of their phenotypic correlations across time. Thus, a
substantial proportion of the phenotypic associations between
cognitive development and cognitive stimulation can be attributed to
bidirectional causal effects, while shared etiology or common causes
– in particular, the shared environment – accounted for the
remainder of the correlations. Finding that common causes and
bidirectional causal effects jointly explain the associations between
cognitive development and cognitive stimulation is key for developing
realistic expectations for the magnitude of the effects that
early-life interventions can possibly achieve (von Stumm, 2022).
We also showed that children’s
differences in cognitive development and stimulation are largely due
to shared environmental influences (56%-74%), followed by additive
genetic influences (24%-40%). A similar pattern emerged for the
etiologies of the associations between cognitive development and
stimulation, which were again mainly due to shared environmental
(76%-83%) and then additive genetic influences (16%-20%). Non-shared
environmental influences on cognitive development and cognitive
stimulation were negligible. While this study is to our knowledge the
first to estimate the heritability of cognitive stimulation and its
association with cognitive development, our findings confirm that all
traits are heritable, including putatively environmental measures
that are genetically influenced (Krapohl et al., 2017; Plomin, 1995;
Polderman et al., 2015).
Limitations
Notwithstanding this study’s many
strengths, including the analysis of twin and genomic data, large
sample sizes, and repeated assessments of the core constructs using
state-of-the-art methods, it is not without limitations. First,
cognitive stimulation was assessed using seven parent-reported items,
but a multi-informant approach (i.e., naturalistic home observations)
with a greater number of observed variables would have improved the
measures’ validity. Second, data on cognitive stimulation were only
collected at the twins ages 3 and 4 years, which made it impossible
to test for meaningful changes in the direction of causality over the
longer course of childhood. Third, the association between the PGS
for years spent in education (Lee et al., 2018) and cognitive
development was small, which is indicative of weak instrument biases
that can lead to overestimation of causal effects (Burgess &
Thompson, 2011). In addition, cognitive development and cognitive
stimulation did not have a sufficiently differentiated genetic
architecture to meet the assumptions of DoC models (Health, 1993; van
Bergen et al., 2018). As a result, our preregistered analysis
strategy was not viable, and we fitted cross-lagged twin models
instead that require longitudinal data.
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