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To date, research shows that the genetic etiology of reading disability is not dissimilar to that observed for the normal range, supporting the generalist genes hypothesis (Plomin and Kovas 2005). However, findings on the genetic etiology of reading disability in boys versus girls are mixed. Some observe greater heritability in boys (Harlaar et al. 2005; Stevenson 1992), while others do not (Wadsworth and DeFries 2005). We explored these issues for reading measured with the TOWRE at Grade 1 with a dataset compiled across Australia and the US. The full distribution of the sample comprised 413 MZs and 420 DZs. The top and bottom probands were those with scores greater than 1 SD either above or below the mean. For the bottom proband, the estimates of A, D, C and E were 53, 0, 26 and 21%; for the full distribution they were 77, 0, 7 and 16%; and for the top proband they were 72, 17, 0 and 11%. Through not significant, this shows a trend whereby, when explaining differences between high end reading ability and the normal range, genetic effects were more important, but when explaining differences between reading disability and the normal range, environmental effects played more of a role. While inconsistent with previous research, our trend may be from detrimental environmental effects that impact low but not high end reading ability, rather than differential genetic effects, so our results are not inconsistent with the generalist genes hypothesis. An analysis of the bottom proband separately for males and females showed slightly stronger genetic effects in males (effects of A, C and E were 45, 21 and 24%) than females (effects of A, C and E were 63, 21 and 16%). These differences were not significant thought were in the same direction as Harlaar et al. (2005) and Stevenson (1992) but not Wadsworth and DeFries (2005). |
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