Comorbidity between verbal and non-verbal cognitive delays in 2-year-olds:a bivariate twin analysis

Citation
S. Purcell et al., Comorbidity between verbal and non-verbal cognitive delays in 2-year-olds:a bivariate twin analysis, DEV SCI, 4(2), 2001, pp. 195-208
Citations number
37
Categorie Soggetti
Psycology
Journal title
DEVELOPMENTAL SCIENCE
ISSN journal
1363755X → ACNP
Volume
4
Issue
2
Year of publication
2001
Pages
195 - 208
Database
ISI
SICI code
1363-755X(200105)4:2<195:CBVANC>2.0.ZU;2-V
Abstract
The purpose of this paper is to investigate the genetic and environmental a etiology of the comorbidity between verbal delay and non-verbal delay, in i nfancy. For more than 3000 pairs of 2-year-old twins born in England and Wa les in 1994, we assessed verbal (vocabulary, V) and non-verbal (non-verbal, P) performance. V delay probands were selected who were in the lowest 5% o f V; P delay probands from the lowest 5% of P. We assessed the comorbidity of delay both categorically, using twin cross-concordances, and dimensional ly, by applying a bivariate extension of DeFries and Fulker (DF) group anal ysis. Both approaches are bidirectional, in that probands can be selected f or either V delay (and analysed in relation to their co-twin's P score) or P delay (analysed in relation to their co-twin's V score). From a categoric al perspective, twin cross-concordances indicated that comorbidity between V delay and P delay is substantially due to genetic factors whether proband s are selected for V delay or for P delay. MZ and DZ cross-concordances wer e 24% and 8%, respectively, for probands selected for V delay and 27% and 6 % for probands selected for P delay. From a dimensional perspective using b ivariate DF analysis, selecting for V delay yielded high bivariate group he ritability (0.59) and a genetic correlation of 1.0. In contrast, when selec ting on P, DF analysis indicated lower bivariate group heritability (0.20) and only a modest genetic correlation with V assessed dimensionally (0.36). These results are discussed in terms of the difference between categorical and dimensional approaches to quantitative traits and the bidirectional na ture of comorbidity. Such multivariate genetic results could lead to diagno stic systems that are based on causes rather than phenotypic descriptions o f symptoms.