01 NRDC Dyslexia 1-88 update - Texthelp

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Research Report
Within such a multiple-gene model, it no longer makes sense to think of individuals as
‘dyslexics’ or ‘non-dyslexics’, unless in the sense that their scores fall either side of a
pragmatic threshold on a reading ability test. Accordingly, it does not appear that any genes
‘for dyslexia’ could be simply abnormal variants of genes for normal reading (Davis et al.,
2001).
Abnormalities in myelination and the synthesis of fatty acids in the brain have been proposed
as explanations of processing difficulties in dyslexia and other disorders (Horrobin et al.,
1995; Richardson & Ross, 2000; Stordy, 2000; Taylor et al., 2000), but the links between
dyslexia and any genes coding for errors in protein synthesis are still conjectural (Francks et
al., 2002; Habib, 2000). For example, a link between dyslexia and an abnormality in a gene
that codes for a protein found in myelin has been suspected but not so far confirmed (Smith
et al., 2001), although it cannot yet be ruled out (Turic et al., 2003).
The complexities in this field of enquiry are challenging (Ahn et al., 2001; Asherson & Curran,
2001; Gilger et al., 2001; Grigorenko, 2001; Grigorenko et al., 1997; Rutter, 2002; Wood &
Grigorenko, 2001) and repay greater consideration than is possible in this review. As
elsewhere, the interpretation of research findings is made difficult by the inconsistency of
protocols for identifying research participants, in both quantitative genetics and molecular
genetics studies. These protocols, which not infrequently employ IQ-discrepancy methods,
may limit the applicability of research findings so far as adult literacy students are concerned.
Although it has long been recognised that dyslexia may be familial, a familial trait may also be
transmitted culturally (Pennington, 1991). Thus, contrary to what practitioners may
sometimes suppose, family relationship (‘familiality’) alone is not a reliable indicator of
genetic heritability. (As the Mitford daughters observed, whether by nature or nurture, they’d
had it.)
Familiality in reading disability may have a stronger genetic component among abler people
but a stronger cultural component among the less able, where the two groups also differ in
terms of parental education, books in the home and the extent to which the parents read to
their children (Wadsworth et al., 2000). In any population, the degree of genetic influence on
individual differences depends partly on the range of the relevant environmental influences
(Gayán & Olson, 2003). Reading disability studies where the participants come from the whitecollar
classes will produce higher estimates of heritability than would be expected from more
broadly representative studies with both white- and blue-collar participants.
Policies to optimise home and school environments for learning how to read and write cannot
eliminate all differences between individual outcomes and might not even narrow the range of
outcomes, although they will unquestionably raise the average level of achievement.
Meanwhile, in many countries the single most powerful predictor of literacy achievement is
the number of books in the home (Elley, 1994). This is ostensibly an environmental measure,
although it is doubtless influenced by parental genes.
Although reading difficulties are heritable, no single gene creates a qualitative difference
between dyslexic and non-dyslexic people.
Instead, a number of genes may be involved, each making a quantitative contribution to the
variance in reading and writing ability in the population.
The processes by which these genes take effect are not yet understood.