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Gene × Environment interactions in speech sound disorder predict language and preliteracy outcomes

Published online by Cambridge University Press:  11 October 2007

Lauren M. McGrath ,
Bruce F. Pennington ,
Erik G. Willcutt ,
Richard Boada ,
Lawrence D. Shriberg  and
Shelley D. Smith
Lauren M. McGrath*
Affiliation:
University of Denver
Bruce F. Pennington
Affiliation:
University of Denver
Erik G. Willcutt
Affiliation:
University of Colorado at Boulder
Richard Boada
Affiliation:
University of Colorado at Denver
Lawrence D. Shriberg
Affiliation:
University of Wisconsin–Madison
Shelley D. Smith
Affiliation:
University of Nebraska
*
Address correspondence and reprint requests to: Lauren M. McGrath, University of Denver, Department of Psychology, Frontier Hall, 2155 S. Race Street, Denver, CO 80209; E-mail: [email protected].
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Abstract

Few studies have investigated the role of gene × environment interactions (G × E) in speech, language, and literacy disorders. Currently, there are two theoretical models, the diathesis–stress model and the bioecological model, that make opposite predictions about the expected direction of G × E, because environmental risk factors may either strengthen or weaken the effect of genes on phenotypes. The purpose of the current study was to test for G × E at two speech sound disorder and reading disability linkage peaks using a sib-pair linkage design and continuous measures of socioeconomic status, home language/literacy environment, and number of ear infections. The interactions were tested using composite speech, language, and preliteracy phenotypes and previously identified linkage peaks on 6p22 and 15q21. Results showed five G × E at both the 6p22 and 15q21 locations across several phenotypes and environmental measures. Four of the five interactions were consistent with the bioecological model of G × E. Each of these four interactions involved environmental measures of the home language/literacy environment. The only interaction that was consistent with the diathesis–stress model was one involving the number of ear infections as the environmental risk variable. The direction of these interactions and possible interpretations are explored in the discussion.

Type
Research Article
Information
Development and Psychopathology , Volume 19 , Issue 4 , Fall 2007 , pp. 1047 - 1072
Copyright
Copyright © Cambridge University Press 2007

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