A recent study has found both a physiological cause for dyslexia, as well as a solution. Is it too good to be true?
Dyslexia is a remarkably common affliction. Indeed, dyslexia is so common that it affects approximately 10 per cent of the Australian population. Classified as a type of specific reading disability, dyslexia is a neurodevelopmental disorder that presents as problems with reading, writing and spelling that is usually first noticed during childhood — when these skills are being learned.
Despite its prevalence, little is known about the potential cause or causes of dyslexia. To date, best guesses have been that genes and heredity play a role, potentially as well as structural differences in areas of the brain involved with reading skills. There is also some evidence that premature birth, low birth weight, and prenatal exposure to drugs, alcohol or infection may increase the likelihood of dyslexia.
This sets the stage to sculpt a fairly grim picture (the more literary among you may note I have cleverly alluded to recent research showing an inclination towards creativity in those with dyslexia), as it seems a child’s chances of being diagnosed with dyslexia are a result of factors largely beyond their control, and therefore unmodifiable. A diagnosis of dyslexia may also be accompanied by a swathe of other issues, such as problems keeping up with peers, low self-esteem, anti-social behaviour, and attention-deficit hyperactivity disorder (ADHD).
But what if there were another, previously unidentified, cause of dyslexia? A physiological cause, with a potential solution? Wouldn’t that be wonderful news?
Well, researchers from the Laboratory of Laser Physics at the University of Rennes in France believe that this might be the case. Researchers identified differences in the arrangement of cells that absorb light in the eyes of those diagnosed with dyslexia, compared to those without such a diagnosis. The human retina consists of two types of photoreceptors: rods and cones. Rods are useful for seeing things in low light, but can’t distinguish colour. Cones can be red, green or blue, facilitate colour vision, and are best in bright light.
The majority of cones are in the fovea, which is a small spot at the centre of the retina. Within the fovea, there is a tiny region which contains only red and green cones, no blue cones allowed. These researchers found that the arrangement of cones in this particular area seemed to differ between individuals with and without dyslexia. In people not affected by dyslexia, cone cells were arranged asymmetrically and so each eye received slightly different visual input. The brain chooses which eye it ‘believes’, so to speak, and this eye becomes the dominant eye.
In those affected by dyslexia, the blue-cone-free spot appeared symmetrical in both eyes, suggesting that no eye could gain dominance. The researchers propose that this results in the visual perception of mirror images where they don’t actually exist, for example a ‘b’ looking like a ‘d’. The researchers also reported a brief delay in the brain’s receipt of input from each eye, allowing them to override one of the images by exposing participants to a fast-flashing LED lamp, and apparently ‘fixing’ the mirror image issue.
On the face of it, these findings seem remarkable. They offer both a physiological cause for dyslexia, and a solution. The study was published in a biological sciences journal, Proceedings of the Royal Society B, and has received significant media attention (including, but not limited to, this very article).
However, as is so often the case, all that glitters is not gold, and neither is all that gets published. The limitations of the study are significant. To start, the study has a small sample size (only 30 people with dyslexia, and 30 without), which reduces the chances that these findings apply to the broader population. There is also limited neurological evidence for the underlying premise of ‘mirroring’, with this frequently being labelled a ‘neuromyth’.
Most significantly, these findings seem to have fallen into the common pop-science trap of assuming causation where there is only correlation. That is, do people with a symmetrical arrangement of cones in the fovea develop dyslexia, or does the experience of having dyslexia lead to a symmetrical arrangement of cones in the fovea? I’m sure we’ve all puzzled over this very question on more than one occasion.
And finally, does the research pass the common-sense test? Does it have face validity? If these findings hold up, how many people can “fix” their dyslexia by reading with a patch over one eye?
Dr Jessica L Paterson, Senior Research Fellow, CQUniversity, Appleton Institute