John Stein outlines his research suggesting that simple visual treatments and omega-3 fish oils can significantly improve the reading ability of dyslexics

Every few years somebody resuscitates the view that developmental dyslexia does not exist at all, but is a middle class excuse for their children’s laziness or stupidity. A current version is that, since all backward readers benefit from instruction in splitting words down to their constituent sounds (phonics), there is no reason to distinguish dyslexia from other causes of reading problems, such as poor teaching or low intelligence. This is just another way of saying dyslexia does not exist, and it is dangerously wrong on two counts.

First, developmental dyslexia has many other features than just poor reading, including a proven genetic basis and distinct neurological features, such as impaired activation of left sided areas involved in speech and reading compared with good readers. It is also characterised by impaired sequencing and poor short term memory in tasks not necessarily involving reading at all, such as reciting the days of the week or months of the year. To ignore these facts is cruel and dangerous because it may deprive children of the help they deserve and need.

Second, it is quite untrue to claim that all poor readers benefit from phonological instruction. Everybody who actually teaches dyslexics knows that despite intensive phonics training, there remains a substantial proportion who fail to benefit at all. Many of these complain that they cannot see the letters properly on the page because they blur, move around or change their order. Such oscillopsia is common after lesions of the cortical occipito-temporal area or cerebellum, which are acquired causes of reading problems. Both areas have also been implicated in developmental dyslexia. We have found that up to two thirds of all the children we see have such visual symptoms that may help to explain their reading problems.

These problems are not surprising, since vision is the main sense used for reading. When we are learning to read, we have to learn to identify each letter or group of letters visually in the right order and then translate them into the sounds they stand for. But in practised readers this auditory translation is unnecessary; whole words are recognised visually and their meaning extracted directly.

We now know that all these visual processes depend greatly on the proper function of a set of large visual neurones, called magnocells, that time visual events and respond rapidly to visual motion. Because they feed back any unwanted visual motion on the retina to the servo system that keeps the eyes on target, they are extremely important for maintaining stable visual perception of letters, and preventing them appearing to move around.

Many dyslexics have been shown to have impaired development of this visual magnocellular system. Neuropathologically, this has been demonstrated by examining these nerve cells post mortem. But also in life, their defects have been shown using electrophysiological and psychophysiological techniques that selectively activate magnocells in the retina and along the pathways through the visual cortex to the posterior parietal cortex, and also by functional imaging. This mild magnocellular impairment leads to poorer attentional and fixation stability in dyslexics, hence their visual reading problems. 90 per cent of recent research that has examined the role of the magnocellular system in dyslexics concurs that most have such a deficit. Its mildness means that you need sensitive tests to detect it. Unfortunately, this has meant that it has been possible for those who still believe that dyslexia is largely a linguistic phonological problem to ignore this evidence completely. This is very bad for the large numbers of children with visual magnocellular deficits leading to visual reading problems, because it deprives them of the simple techniques we can use to help them.

The simplest is to get them to read through either deep yellow or blue filters. We have tested a variety of other colours supplied by manufacturers, who claim that up to 2000 colours need to be used to properly treat each individual child, and we have found that just yellow and blue suffice. Yellow and blue probably work in different ways. Magnocellular neurones in the retina receive their main input from the red and green cone receptors, so yellow filters, which allow red and green but not blue light to pass through to the receptors, slightly boost the output of the magnocells. This is often enough to relieve children’s symptoms. In a randomised controlled trial, we showed that yellow filters could increase dyslexic children’s reading by six months after three months of wearing them, compared with only two months in those receiving placebos.

Blue filters seem to work differently. The peak transmission of our Oxford blue filters is 450 nanometres, so they cut out most red and green light; hence, they do not stimulate magnocells directly. Instead, they activate a new kind of retinal cell that has recently been discovered to contain melanopsin, a pigment maximally stimulated by blue light. These input, not to the conscious visual cortex, but to the suprachiasmatic nucleus in the hypothalamus. This nucleus contains our body clock which times our arousal and sleep. It needs to be synchronised to seasonally changing day length and so the retinal melanopsin cells switch it on earlier in the summer and later in the winter. The main system switched on during such arousal is our system of magnocellular nerve cells. Thus, our blue filters help dyslexics by facilitating their magnocellular arousal. Not only do they help reading in susceptible children even more than the yellow filters do in other children, but they also improve poor sleep patterns. Serendipitously, we discovered that the blue filters can also reduce the children’s migraine headaches, probably because diurnal malfunction of the cortical pain system that causes migraine is also controlled by the suprachiasmatic clock.

Thus, we can help half of children with reading difficulties with these very simple visual treatments. But there remain a significant number of children who do not have visual problems of any sort. These are the children who get word sounds in the wrong order, tend to mispronounce long words, and who therefore have particular problems with phonology. The cues that enable letter sounds to be distinguished are rapid changes in sound frequency and amplitude. Tracking these is the function of the auditory equivalent of the visual magnocells, and there is now much neuropathological, psychophysical and functional imaging evidence that many dyslexics have impaired development of these auditory magnocells.

Clearly, this contributes to their phonological problems. But concentrating on their weaknesses by bludgeoning them with phonics training does not seem to help them much. Yet various programmes teaching children rhythm and tune do seem to help their auditory processing to develop better, which then generalises to improve their phonological skills.

Although auditory magnocells do not constitute such a readily recognisable separate network as in the visual system, we find magnocells devoted to timing events in all parts of the nervous system: in the frontal lobe, in the cerebellum, the body’s autopilot, and in the hippocampus, the main memory system. They can be recognised by their size and by their expressing a specific signature molecule (known as CAT 301) on their surfaces that enable them to recognise each other and respond correctly to migration commands.

KIAA 0319 is a gene on the short arm of chromosome 6 that we have discovered from genetic linkage studies in our local dyslexic families to play an important part in reading. If this gene is experimentally knocked out completely, neurones fail to migrate at all. Thus, it seems that it controls the way nerve cells migrate, setting up the processing networks in the brain early in development. In dyslexia, this gene is slightly down regulated, which could explain why magnocells fail to develop properly and do not migrate to quite the right places.

Another gene that we have implicated in dyslexia is one that contributes to the metabolism of long chain omega 3 polyunsaturated fatty acids (LCPUFAs) which we normally gain from eating oily fish. This is significant to the magnocellular theory because magnocells need to have flexible cell membranes that allow their ionic channels to open and close fast. 50 per cent of the membrane is made of a single LCPUFA derived from oily fish, docosahexaenoic acid (DHA). Because it is kinky, and does not pack together densely, magnocellular membranes are flexible and can react fast.

But DHA is also used for other things and it is continuously leeched out of the membrane. So magnocells are extremely vulnerable to lack of DHA and also to another LCPUFA, eicosapentanoic acid (EPA), that is important for intercell signalling. Our modern diet is dreadful, with too much salt, sugar and fat, and too little oily fish, minerals or vitamins, hence a high proportion of the population is dangerously deficient in these essential nutrients. In randomised controlled trials we have shown that giving children supplement capsules containing EPA & DHA from oily fish can dramatically improve their magnocellular function and, therefore, their ability to focus attention and to improve their reading.

What we also found was that these children’s mood and behaviour also improved greatly and we have put this to good use in prisons. Simply giving young offenders supplement capsules of fish oils, minerals and vitamins reduced their rate of offending in prison by over a third. We are now completing a much larger study hopefully to prove conclusively that simply improving these young men’s diets can help them to control themselves more effectively and therefore to behave less antisocially. If such a simple and cheap solution really is that powerful, it will have profound implications.

Further information

John Stein is Professor of Neurophysiology at University of Oxford and Chair of the Dyslexia Research Trust: