Yet another Ritalin horror story hits the headlines! It seems that every week I can open a newspaper, or magazine, or turn on my PC, and be faced with another story, or article, or news headline, in which I am informed of the the increasing trend in incidence of children with neurodevelopmental disorders (autism, dyslexia, ADHD and dyspraxia). Given the repeated message of the side effects experienced by these children outweighing the benefits, the rise in the number of children routinely taking pharmaceutical drugs, like Ritalin, is both concerning and alarming. Why is it that these pharmaceutical offerings continue to be dished out, and why are parents not informed of alternative treatments that are not only are proven to work, but also come without side effects?
There has been a twelve-fold increase in autism over the last 30 years, and it would be easy to relate this to changes in food processing methods and the corresponding impact on our children’s diets. An association does not, however, necessarily imply cause, and care must be taken when making such statements. Indeed, whilst more research is certainly needed to confirm the dietary link to such conditions, some scientists seem almost reluctant to admit that such a concept is even plausible. For much of its history, autism has been considered a discrete psychological disorder, managed largely with behavioural intervention techniques. However, many studies have outlined, with great interest, its co-morbidity with other neurodevelopmental disorders, such as ADHD, dyslexia and dyspraxia, where pharmaceutical intervention is a given part of the treatment. A common feature existing in children with neurodevelopment disorders is the specific differences and/or deficiencies in the type of fats (phospholipids) that make up their nerve cell membranes. It has been suggested, and shown, in many well structured trials, that supplementation with specific fatty acids can not only rectify deficiencies, but also be used as a safe alternative to drugs such as Ritalin.
Phospholipids are a major component of every cell membrane, including nerves. Made up of a stabilising ‘polar head’ coupled with fatty molecules, the phospholipid content, and in particular the specific type of phospholipid within nerve cell membranes, dictates many cell functions. A dysregulation in phospholipid
metabolism, as has been suggested in neurodevelopmental disorders, would have a profound influence on brain processes, and may account for many of the symptoms. Phospholipids are constantly being synthesised and broken down, and whilst the enzymes responsible for this normal turnover are under genetic control, the key essential fatty acids of neuronal phospholipids must come from the diet.The type of fat consumed, therefore, can have a profound effect on neurone function, and consequently brain function.
The two major polyunsaturated fats with the brain are the omega-6 AA and omega-3 DHA, which account for around 20% of the dry brain weight. DHA is known to be involved in cell signalling and has an important structural role in the brain, whilst AA is crucial for brain growth. EPA, another major omega-3, is present in most cell membranes, though it has little structural role within brain neurones. However, unlike DHA, EPA is considered vital for the regulation of brain function and not only converts to DHA, but also protects membrane DHA from breakdown through influencing the phospholipase enzymes that act like scissors and are involved in the release of DHA from membranes. Overactive phospholipase enzymes can release DHA unnecessarily and therefore sufficient EPA must be present in the diet, not only to protect detrimental loss of DHA from neurones but also to ensure that the brain functions normally.
The dysregulation in phospholipid metabolism believed to occur in children with neurodevelopmental disorders is thought to be two-fold, firstly, through an increased turnover of the phospholipid membrane, and secondly through a reduced capacity to replenish the phospholipid membrane. Either would result in disruption of the membrane’s normal structure, a combination would have more severe consequences. As humans have a low capacity to synthesise long-chain fatty acids, they must rely on dietary sources such as fish, or fish oils, to meet demands. Low dietary intake of long-chain omega-3 will exacerbate the condition and, understandably, supplementation with long-chain omega-3 will be beneficial. There have been numerous trials investigating the use of ‘fish oils’ in neurodevelopmental disorders and, whilst not all results have been favourable, it appears that the lack of clear and decisive results have been due to the choice of oil used, the dose, and the trial length. For example, given that fatty acid supplementation may take up to 3 months to substantially inﬂuence fatty acid deﬁciencies, it may not be appropriate to look for behavioural changes immediately upon commencing supplementation. Dosage is also key; it appears that for a supplement to have both neuroprotective and neuroregulatory actions, the amount of actual long-chain omega-3 needs to be higher than present in most common generic oils, and that the ratio of EPA to DHA needs to be higher than is typical of these oils. Using pure ethyl-EPA at a dose of 0.5-1.0g, for a period of at least three months is currently the most favoured and proven supplementation regime for treating neurodevelopmental disorders: a regime that not only offers other health benefits, but is easy to implement and with no unpleasant side effects. It’s time to open our eyes to the possibility that pharmaceutical drugs are not always the answer and that, as parents, we have the right to choose the best and safest treatment to help our children.