Introduction-Attention-deficit/hyperactivity disorder (ADHD) and reading disability (RD) are complex childhood disorders that frequently co-occur, but the etiology of this comorbidity remains unknown.Method-Participants were 457 twin pairs from the Colorado Learning Disabilities Research Center (CLDRC) twin study, an ongoing study of the etiology of RD, ADHD, and related disorders. Phenotypic analyses compared groups with and without RD and ADHD on composite measures of six cognitive domains. Twin analyses were then used to test the etiology of the relations between the disorders and any cognitive weaknesses.Results-Phenotypic analyses supported the hypothesis that both RD and ADHD arise from multiple cognitive deficits rather than a single primary cognitive deficit. RD was associated independently with weaknesses on measures of phoneme awareness, verbal reasoning, and working memory, whereas ADHD was independently associated with a heritable weakness in inhibitory control. RD and ADHD share a common cognitive deficit in processing speed, and twin analyses indicated that this shared weakness is primarily due to common genetic influences that increase susceptibility to both disorders.Conclusions-Individual differences in processing speed are influenced by genes that also increase risk for RD, ADHD, and their comorbidity. These results suggest that processing speed measures may be useful for future molecular genetic studies of the etiology of comorbidity between RD and ADHD.
We report preliminary behaviour genetic analyses of reading and listening comprehension from The Colorado Learning Disabilities Research Center. Although the twin sample with these new measures is still of limited size, we find substantial, and significant, genetic influences on individual differences in both reading and listening comprehension. In addition, word recognition and listening comprehension each accounted for significant independent genetic influences on reading comprehension. Together, they accounted for all the genetic influence on reading comprehension, indicating a largely genetic basis for the 'simple model' of individual differences in reading comprehension proposed by Hoover and Gough (1990).When we began our behaviour genetic studies of 'dyslexia', or reading disability, with identical and fraternal twins in 1982, it was commonly assumed that the difficulties in reading comprehension that children with dyslexia have are largely, if not completely, because of their deficits in phonological skills and word decoding (Liberman, Shankweiler, Fisher & Carter, 1974;Perfetti, 1985;Shankweiler, 1989). For example, in Perfetti's 'verbal efficiency theory', the higher processing demands in word decoding in poor readers were thought to result in fewer resources for processing the meaning of text, resulting in deficits in their reading comprehension. However, in recent years, evidence has been accumulating to support some dissociation between decoding and comprehension problems. This raises the question of the extent to which deficits in decoding and comprehension share a common aetiology. The purpose of this report is to provide preliminary findings in our attempt to address this question by examining the genetic and environmental aetiologies of individual differences in comprehension.
Relation between word decoding and comprehension problemsEarly research by Curtis (1980) found that while word decoding and reading comprehension are very highly correlated in beginning readers, this correlation declines
We examined reading comprehension in children with ADHD by assessing their ability to build a coherent mental representation that allows them to recall central and peripheral information. We compared children with ADHD (mean age 9.78) to word reading-matched controls (mean age 9.89) on their ability to retell a passage. We found that even though children with ADHD recalled more central than peripheral information, they showed their greatest deficit, relative to controls, on central information – a centrality deficit (Miller & Keenan, 2009). We explored the cognitive underpinnings of this deficit using regressions to compare how well cognitive factors (working memory, inhibition, processing speed, and IQ) predicted the ability to recall central information, after controlling for word reading ability, and whether these cognitive factors interacted with ADHD symptoms. Working memory accounted for the most unique variance. Although previous evidence for reading comprehension difficulties in children with ADHD have been mixed, this study suggests that even when word reading ability is controlled, children with ADHD have difficulty building a coherent mental representation, and this difficulty is likely related to deficits in working memory.
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