Current Trends in Nutrition

The Role of Omega-3 Nutritional Supplements in Treating Childhood Dyslexia
Dyslexia is a literacy disorder whose exact cause remains unknown. It does not affect IQ or other cognitive function, but can profoundly impair reading ability. It is believed that heredity plays a role, and several studies have sought to determine whether degree of deficiency of fatty acids in the diet could also be a contributing factor ( Richardson AJ, 2000). Dyslexia has been linked to clinical signs of fatty acid deficiency in adults, so the question of treating developmental dyslexia in children with fatty acid supplements has been raised as a possible safe and effective treatment (Taylor KE, 2000). There is a growing trend among holistic practitioners and drug manufacturers alike, to develop and market supplements to treat dyslexia, and as the disorder has such far-reaching consequences in academic success, self-esteem, and social interaction for those who suffer from it, the market is quite receptive to new treatment approaches. (Evans R 1999)
Given that development of nutritional dyslexia treatment is a relatively new endeavor in the scientific community, review of current and recent research on the matter is appropriate. Evaluating proposed treatments and commercially-prepared nutritional supplements will be more effective with a background understanding of the issue.
Research studies have reported that dyslexic children are deficient in body stores of zinc, and that their sweat contains a far less amount of zinc that non-dyslexic children (Grant ECG 1989). Research also indicates that low maternal zinc levels can predict dyslexia in a fetus, and that maternal zinc supplementation can greatly reduce the occurrence of dyslexia, even when a strong genetic predisposition for dyslexia exists (Ames B 2004). Zinc appears to work with B vitamins and enables the body to absorb and use the important essential fatty acids. Zinc deficiency is believed to block essential phospholipid pathways, resulting in reduced incorporation of docosahexaenoic acid and arachidonic acid into cell membranes. But while zinc deficiency has frequently been observed in dyslexic patients, current nutritional remediation efforts are largely focused on essential fatty acid supplementation.
A study by Lien and Clandinin used a three-day food record to quantify dietary consumption of arachidonic acid (AA) and docosahexaenoic acid (DHA) in healthy 4-7 year olds (Lien V 2009). On the basis that children with ADHD and other learning disorders have lower AA and DHA levels, they sought to evaluate this problem from a different angle, by better defining how much AA and DHA a typical healthy child consumes in their diet.
Children and parents were instructed to keep a three-day food record. The population of 91 subjects studied did not live near the coast, which could have affected their intake of fish, and all children were of normal intellectual ability for their age. Other potential confounding variables were not considered because the purpose of this project was simply to get a broad picture of the amount of essential fatty acids that children regularly consume. The issues of cause and effect were not directly considered.
The hypothesis that children consume low intakes of essential fatty acids in their diets was supported by the results obtained. It was determined that the AA and DHA intake of these children was approximately 1/15th of the level received by breastfed infants. This study illustrates just how little AA and DHA the typical western diet provides, and gives a basis for further research into the benefits of essential fatty acid supplementation. Lindmark and Clough studied the effects of essential fatty acid, or EFA, supplementation on the reading ability of dyslexic children in Sweden and had very promising results (Lindmark l 2007). In an open, non-random study, they sought to test a specific nutritional supplement, called Efalex, to see if it could help improve reading skills in dyslexic children. The supplement was provided free for this 5-month study by the manufacturer. Participants were instructed to take 8 capsules per day, which amounted to 480mg of DHA, 108mg of EPA, 96 mg of GLA, and 35 mg of AA. The null hypothesis was that EFA supplementation does not affect reading ability in dyslexic children, and the alternate hypothesis was that EFA supplementation improves reading ability in dyslexic children.
Inclusion criteria were that all children in the test group had been formally diagnosed as dyslexic and were recruited from a dyslexia support group near Stockholm, Sweden. They were all given word-chain reading tests that placed them below normal in reading ability. Exclusion criteria included fish allergy, and only data from those students who completed the entire treatment regimen were included in the results. There was no ethics approval required for this study, but informed consent was obtained from parents.
After 4 months of supplementation, the word-chain test was administered again, and 76% of participants demonstrated a measurable increase in reading ability. In the study overall, the subjects’ word recognition scores improved by 23% over the 4 month period, and reading speed improved by 60%.
Subjective evaluation forms were filled out by parents after 6 weeks and 12 weeks, and showed that more parents perceived their child’s readily ability had improved as time progressed. After 6 weeks of treatment, 26% of responders perceived a positive effect, but by 20 weeks that number had increased to 89%. After 5 months of supplementation, a subjective interview was performed, which showed that both children and parents reported seeing significant reading improvements over the course of the study. The duration of the study was adequate in measuring this gradual improvement in reading ability.
While the results are impressive, the study was not randomized, which would have helped to minimize the effects of any confounding variables. The study design and research setting made it difficult to control for extraneous variables, although the study authors feel their results indicate such a high level of reading improvement in these children that potential sources of confounding cannot account for the dramatic results completely. In other words, whether or not other variables were tightly controlled, they feel their alternate hypothesis was supported. They did attempt to control other factors to some degree by performing the study during the summer to minimize the effect of school on improving reading skills, for example, and although there was no placebo-controlled group in the study, they describe the potential for placebo effect in their study as negligible due to the months-long duration of the project. There was also an attempt made to control bias by interviewing children and parents separately and questioning the children first.
The reading measurements used were appropriate and commonly utilized by educators to evaluate reading ability, whether or not a child is dyslexic. They were performed properly, and the statistical results of this study were correctly interpreted. While the results are very encouraging for the treatment of dyslexia with EFAs, further study is necessary with placebo-controlled trials to help substantiate these results.
Since the intake of omega-6 polyunsaturated fatty acids, or PUFAs, is generally much higher than necessary in the modern diet, and since omega-3 fatty acids are often lacking, administering omega-3 PUFAs to dyslexic children seems a wiser choice than using a supplement also containing omega-6 PUFA. To be clear however, the subjects in this study did not have their omega-3 or omega-6 levels tested prior to beginning the study, so it is unknown if they were deficient prior to supplementation. It is unclear from the results of this study if it was the omega-3 or omega-6 components of the supplement that were responsible for the reading improvements noted. It is not clear whether the benefits of this supplement were from correcting a nutritional deficiency, or from supplementing PUFAs at levels beyond RDAs.
The Oxford-Durham Study is a well-known experiment published in 2005 which demonstrated that EFA supplementation in children increases their reading and spelling abilities, as well as providing marked improvement in behaviors associated with ADHD (Richardson AJ 2005). This study provided 3 months of EFA supplements for 117 children who had been diagnosed with DCD, or developmental coordination disorder, which is a combination of overlapping disorders including dyslexia, ADHD, dyspraxia, and related conditions. The alternate hypothesis was that 3 months of EFA treatment would lead to significant improvements in three measured areas: motor skills, literacy skills, and teacher-rated ADHD behavior, while the null hypothesis was that there would be no difference between the treatment and placebo groups.
The treatment consisted of both omega-3 and omega-6 fatty acids in the form of 558 mg eicosapentaenoic acid (EPA), 174 mg docosahexaenoic acid (DHA), and 60 mg linoleic acid. This treatment was the independent variable in the study, and was given for 3 months in parallel, randomized groups. This was followed by a one-way treatment crossover where those who received the placebo during the first 3 months were then given the treatment regimen.
The outcome measures of motor skills, reading and spelling skills, and subjective teacher-rated level of ADHD symptoms were recorded at baseline, and again at 3 months and 6 months. These were the dependent variables in this study. Statistically significant improvements in reading and spelling skills, as well as ADHD symptoms, were noted with both the primary treatment group and the placebo group after their crossover to active treatment. No improvement was noted with motor skills in any of the study groups, whether receiving the treatment or placebo.
The methods of the study do appear to have been properly performed and well-conceived to maximize the strength of the study. This was a between-subjects design. Power calculations were properly employed in this study to determine target sample size, and a size of 50 subjects per group was chosen to yield >80% power at the 0.05 level. Biases were minimized by the study design. Matching was not used; participants were randomized by computer generated random sequence, and all participants, outcome assessors, and personnel administering the interventions were blinded. The study was approved by the appropriate ethics committee, and written informed consent was obtained from parents.
Other eligibility criteria included permission from the child’s pediatrician and medical history free of other significant ailments, and DCD diagnosis that was verified through baseline testing. Exclusion criteria included potentially confounding medical treatments, other serious medical conditions, and not completing the full course of the study. The length of the study was adequate at 3 months, since this is the time required for EFAs to be built up in the neuronal membranes. However, subjects were recruited from only the first 12 schools in a particular county who were willing to participate, so it is worth questioning how much this study can be generalized to a wider population.
The conclusions drawn by the study’s authors are correct and appropriate. The results show a strong statistical relationship between EFA supplementation and both improved reading and spelling skills and reduced ADHD behavior. While the mean reading and spelling increase was 6.6 in the treatment group, it was only 1.2 in the placebo group. The improvement in ADHD behavior was even more striking; with only 23.5% still meeting the clinical diagnosis criteria for ADHD by the end of the study. While motor skills did improve during the study, there was no mean change in motor skills between the treatment and placebo groups, so the authors are correct to say the part of their hypothesis that states EFA supplementation will also improve motor skills is not supported. Further research should be undertaken to corroborate these findings, and to determine an ideal dose of EFA to obtain positive results.
In another study, Kairaluoma, et al, researched the effects of fatty acids and carnosine on reading abilities of children with reading difficulties (Kairaluoma L 2009). During a treatment period of 90 days, matched groups of children with below-normal reading ability were given 500 mg/day of ethyl-EPA and 400 mg/day of carnosine. Literacy skills were measured before and after treatment through subjective interviews and questionnaires, and standardized reading tests, and plasma EFA levels were checked to verify an increase in the treatment group. The alternate hypothesis was that this EFA and carnosine supplement would improve reading skills; the null hypothesis was that the supplement would have no impact. The results indicate no statistically significant differences between placebo and treatment groups in this study, and thus the authors state that EFA supplementation does not improve reading skills in dyslexic children.
This was a double-blind study in which participants and researchers were blinded until analysis of the results. The intervention period occurred during the school year, and the study did not control for the variable of reading improvements caused by learning in school, rather than by the supplements. The study received ethics committee approval and informed consent from parents. The independent variable in the study is reading skills, and the dependent variable is the supplements of EFA and carnosine given to the treatment group.
These authors say the Oxford-Durham study cannot be generalized to dyslexia specifically, since the study participants had Developmental Coordination Disorder (DCD), which is a combination of dyslexia, dyspraxia, and ADHD symptoms. However, in practical terms, dyslexia does co-occur with these related problems quite frequently, and recruiting subjects for a trial of EFA treatment on children without these co-occurring disorders would likely be difficult. Their criticism of the Oxford-Durham study is accurate, but this confounding variable appears nearly impossible to eliminate, even though the Oxford-Durham study appropriately used randomization to try to minimize its impact. However, Kairaluoma’s study cannot be compared to dyslexic children in the Oxford-Durham study because the Oxford-Durham treatment protocol only supplemented with EFAs. Kairaluoma administered both EFAs and carnosine to the experimental group.
The inclusion criteria for the Kairaluoma study required a score of 4 or more standard points below grade level on a reading test, and an IQ score above 80. Exclusion criteria included neurological and psychiatric disorders. However, the recruitment of subjects included students with subjective, teacher-observed reading difficulty, but no documented language impairment. Further, students recruited for this study all participated in regular classes, with no mention of remedial reading or tutoring involvement.
It is therefore plausible that the study’s results did not indicate reading improvement with EFA supplementation because the subjects tested did not have dyslexia. The researchers excluded students with neurological disorders, and if this means that those with ADHD, dysgraphia, and dyspraxia were excluded, and given that these disorders commonly occur alongside dyslexia, they likely excluded many dyslexic children from the study as well, particularly since a formal diagnosis of dyslexia was not a requirement to participate in the study. This experiment only required teacher-evaluated reading difficulty, without considering that numerous things other than dyslexia could cause this.
This study does not sufficiently isolate for the effects of EFAs versus the effects of the carnosine included in the treatment regimen. Strangely, the only explanation given as to why carnosine was included in the study was a single sentence stating they believed carnosine can have a positive impact on cognitive function. As other studies have indicated a positive outcome for dyslexic children treated with EFAs, it is possible that this study’s inclusion of carnosine negatively influenced the effect of EFAs. It is also possible that EFAs do improve the reading skills of dyslexic children but this study did not ensure its participants actually had dyslexia, and this is why no reading improvement was noted.
Appropriate statistical tests were used to evaluate the data. The outcome measures in the study were reading and spelling; word and pseudo-word reading; text reading; spelling; decoding fluency; naming; phonological processing; and verbal short-term memory. Additionally, other measures were employed, such as questionnaires and interviews with students, parents, and teachers. Arithmetical skills were also assessed before and after treatment. There is a condition called dyscalculia which involves difficulty with the neurological processing involved in mathematics, and whose incidence overlaps with that of dyslexia in many children. Yet, no mention of screening for dyscalculia is made in this study, and as such, the possible presence of dyscalculia in some of these children is a significant, and unaddressed, confounding variable.
The researchers in this study have not adequately controlled confounding variables, and did not begin the study with a proper set of inclusion and exclusion criteria. This study would have been much more useful and targeted if it tested only EFAs, and not carnosine. Accordingly, the authors are premature to indicate that no relationship exists between EFA supplementation and dyslexia. Further research is necessary.
Generally speaking, EFA supplementation is most likely to help when levels are already low, or a deficiency is present. However, it is not practical or cost-effective to employ biochemical lab testing for EFA levels on a large scale, and other means of detecting this problem are necessary. While not definitive, signs and symptoms such as thirst, frequent urination, and rough or dry patches of skin can be markers of low EFA levels. Fatty acid deficiencies can also play a role in allergic conditions like eczema, hay fever, and asthma, as well as visual perceptual problems and difficulty concentrating. Mood swings and sleep problems may also be present.
While nutrition is undeniably a factor, it is important to note that no single cause of dyslexia has been determined. There does seem to be a hereditary component, but how much weight can be given to genetic predisposition is still the subject of debate. It is known that the final expression of a genetic predisposition to dyslexia depends upon factors in a child’s environment. In sets of identical twins, dyslexia does not always occur in both twins, leading researchers to suspect some form of environmental involvement (Shaywitz S 2003).
Much of the current research about dyslexia centers on functional MRI studies comparing the brains of dyslexics to those without the disorder. Clear differences can be seen with fMRI testing, indicating how dyslexics develop compensatory mechanisms to read using different parts of their brains than do people without dyslexia (Shaywitz S 2003). Significantly, some changes noted with fMRI indicate differences between the brains of dyslexics and non-dyslexics that are present even before children begin learning to read (Raschle N 2012). Mapping these neural pathways has revealed the differences in how dyslexics use their brains to read, and identified which areas of the brain seem to be afflicted. However, research into environmental factors, such as nutrition, need to be further explored.
Copious amounts of anecdotal evidence exist to indicate there is a connection between omega-3 fatty acids and not only dyslexia, but also dysgraphia, dyspraxia, ADHD symptoms, and numerous other neurological impairments. While traditional treatment for dyslexia is measurably effective, the addition of an omega-3 supplement to a dyslexic child’s diet has not shown any detrimental side effects, and should be considered a safe and easy way to potentially improve reading ability. More research is needed to substantiate a definitive, causal relationship and determine optimal omega-3 dosage, and to study what role other nutritional concerns, such as zinc deficiency, play in the development of the disorder.

REFERENCES
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