it has an early onset in childhood and that it is persistent through the life span (although some affected individuals can compensate well and get by, sometimes by avoiding jobs that require significant reading and writing). Building on the knowledge that dyslexia runs in families, twin studies have revealed that it has a genetic basis – identical twins are more similar in terms of their reading and reading disability than non-identical twins. Molecular geneticists have identified some of the many genes associated with dyslexia, but how these interact to cause differences in brain structure and function is not yet understood. Despite this, considerable progress has been made in our understanding of the precursors of dyslexia by studying children who are at family risk of the condition. The findings of such studies reveal that problems in coding the speech sounds of language (phonological skills) are evident from early in the preschool years, long before children are taught to read.
2. People with dyslexia and general poor readers are the same
Until the 1970s, the ‘discrepancy model’ was commonly used as a guiding principle for the diagnosis of dyslexia. Within this framework, dyslexia was identified when there was a significant difference between general intelligence (as measured by IQ) and reading ability6. The discrepancy model differentiated between those readers whose difficulties might be explained by poor education or general low ability – general poor readers – and those whose difficulties could not explained by such factors. Later, as the science of reading developed, this model was retired, better acknowledging that dyslexia existed across the intellectual spectrum7. However, dyslexia’s critics continue to highlight the discrepancy model’s demise as an example of one area where dyslexia science was incorrect, and to suggest that, because it is no longer in use, there is no way to differentiate between those with dyslexia and general poor readers. This is untrue.
While a discrepancy between intelligence and reading ability is no longer considered indicative of dyslexia, other discrepancies remain important. For example, where teachers observe an increasing difference between a pupil’s ability to express herself in writing and in speaking, the presence of dyslexia is suggested8. Moreover, evidence shows that children with dyslexia often show greater resistance to reading interventions (i.e. find them less helpful) than other pupils with reading difficulties. This suggests that the cause of poor reading for some children may not be the same as for others. Such evidence sits alongside the scientific bases for dyslexia, described above. There may not be a universally-accepted dividing line between a pupil with dyslexia, and a pupil without – as with many other difficulties, such as depression, dyslexia exists on a spectrum (see below). Nevertheless, poor reading and dyslexia are not synonymous.
3. All poor readers benefit from phonics-based interventions, so the cause of their difficulties must be the same
Structured phonics-based interventions have been found to be useful to all poor readers. This has been used by critics of dyslexia to suggest that the underlying problem of all poor readers must therefore be the same, i.e. if the treatment is the same, the cause must be the same, too. This argument has two problems. First, as mentioned, while phonics-based interventions have been found to be of use to all, dyslexic readers often show greater resistance to them than other poor readers. Indeed, this is one way that the two groups might be differentiated. Thus, while phonics-based interventions are useful to all, their effects are not uniform, implying that the underlying condition is not uniform, either. Second, as multiple examples attest, the same treatment can be used for quite different underlying problems. Aspirin is sometimes prescribed for those at risk of heart attack, sometimes as an everyday painkiller – in each case, the underlying problem being addressed differs. Identical treatment does not mean identica