Humans require a dietary source of alpha linolenic acid (ALA, C18: 3 (n-3)) and linoleic acid (LA, C18:2 (n-6)). These essential fatty acids are required for the production of eicosanoids, short-lived hormone-like substances that regulate all maner of cell functions including the inflammatory response. Production of eicosanoids is dependent on the conversion of ALA and LA to longer more unsaturated fatty acids in a series of elongation and desaturation reactions. The pathway that leads to the formation of eicosanoids in ALA also produces the long chain fatty acids eicosapentaenoic acid (EPA, C20:5 (n-3)) and docosahexaenoic acid (DHA, C22:6 (n-3)). These fatty acids, particularly DHA, are thought to be necessary for the correct formation of neuronal tissue during development, and deficiency of DHA during adult life is thought to lead to neurological problems because it is a vital component of neuronal cell membranes and as such may facilitate the correct propagation of action potentials.
Understanding the neurological role of the essential fatty acids is difficult because of the ethical problems with depriving humans of essential dietary factors. However, case studies of specific medical cases have been published in the nutritional literature and these are useful in this regard. For example in one study1, a 6 year old girl who had some of her intestine removed, was fed parenterally and her nutritional intake was controlled. After 6 months on a diet that was high in LA but low in ALA she developed neurological problems including numbness, paresthesia, weakness, and inability to walk, pain the legs and blurred vision. An analysis of her serum phospholipid fatty acids was performed and this revealed that she had a marginal deficiency in LA and a serious deficiency of ALA. Addition of ALA to her parenteral feeding regimen reversed the neurological problems. However, re-analysis of the serum fatty acids revealed that while the ALA status of the girl had improved, the LA status had deteriorated.
The original ratio of LA to ALA in the diet of the girl was 115 to 1, while it is estimated that health requires a ratio of around 3 to 1. Six months of consuming the original diet caused a reduction in the concentration of ALA in serum phospholipid of 11.6 %. In addition, the concentration of LA in serum phospholipids dropped to 72 % of that of control children. Therefore the low intake of ALA had resulted in the development of an essential fatty acid deficiency. Further, the high concentration of LA in the diet very likely also suppressed the conversion of ALA to its metabolites in neurological tissues. These factors explain the wide ranging neurological symptoms experienced by the girl. The poor LA status of the girl suggested that other physiological functions may have been perturbed, but LA deficiency is not linked as strongly to neurological problems as that of ALA. The poor LA status in the girl probably does not therefore explain the wide ranging neurological problems.
Dr Robert Barrington’s Nutritional Recommendation: A dietary deficiency of omega-3 fatty acids is very common amongst Westerners. This reflects not only a diet deficient in omega-3 fatty acids, but also a diet high in LA which competes with ALA for desaturase and elongase enzymes and further deteriorates the omega-3 status of the individuals. The typical Western diet is therefore too high in LA and too low in ALA and this results in cellular dysfunction and wide ranging neurological problems. Case studies evaluating the effects of controlled diets in this way are fairly rare in the nutritional literature and can be useful. This this case the presence of a deficiency and an imbalance of essential fatty acids resulted in serious neurological problems. The question therefore arises as to whether a less severe but more chronic deficiency and imbalance have implications for the Western populations as a whole, based on their low quality diet.
RdB
