Abstract
Previous studies have found correlations between parent input and child language outcomes, providing prima facie evidence for a causal relation. However, this could also reflect the effects of shared genes. The present study removed this genetic confound by measuring English vocabulary growth in 29 preschool-aged children (21girls) aged 31-73months and 17 infants (all girls) aged 15-32months adopted from China and Eastern Europe and comparing it to speech produced by their adoptive mothers. Vocabulary growth in both groups was correlated with maternal input features; in infants with mean-length of maternal utterance, and in preschoolers with both mean-length of utterance and lexical diversity. Thus, input effects on language outcomes persist even in the absence of genetic confounds.
Highlights
There is a growing body of research demonstrating that individual differences in children‘s linguistic abilities are correlated with differences in parental speech (e.g., Hart & Risley, 1992, 1995; Hoff, 2003b; Zimmerman et al, 2009)
We previously demonstrated that early language acquisition in this population shows the same qualitative patterns that characterize typical language development, suggesting that similar learning processes may be at work (Snedeker, Geren, & Shafto, 2007)
Like populations of children learning their first language from birth, maternal input significantly correlated with English vocabulary development in IA children
Summary
There is a growing body of research demonstrating that individual differences in children‘s linguistic abilities are correlated with differences in parental speech (e.g., Hart & Risley, 1992, 1995; Hoff, 2003b; Zimmerman et al, 2009). While these studies and others strongly suggest that variation in parental language input contributes to variability in language development, such studies have an unavoidable confound: biological parents provide children with linguistic and genetic input. We conclude by discussing recent findings on the role of genetics in language development and how our results reconcile the gene-environment confound present in previous studies
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