Thus, if fatty acids (and perhaps more specifically, polyunsaturated fatty acids or PUFAs), enhance mitochondrial uncoupling, and if this basic downstream mechanism is responsible for both anticonvulsant and neuroprotective effects (which has yet to be demonstrated), then could taking a chemical uncoupler such as 2,4-dinitrophenol (DNP) render the same effects? Of course, it is well known that DNP, a potent mitochondrial uncoupler that greatly increases the basal metabolic rate, and once used to treat obesity in the 1930’s, has a major untoward side-effect profile – namely, high fever and the risk of death. Clearly, if mitochondrial uncoupling were to represent the essential target, then less potent (and less toxic) compounds are required, and novel delivery systems need to be developed.
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Patricia Daly is a fully qualified Nutritional Therapist (BA Hons, dipNT, mBANT, mNTOI). She is an experienced nutritional therapist and author, specialising in cancer care and the ketogenic diet in particular. She has worked with hundreds of cancer patients in Ireland and abroad, lectures at the Irish Institute of Nutrition and Health and is a well-regarded speaker at conferences and in cancer centres.
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Historically, many anticonvulsant medications have resulted from structural modifications of lead compounds that had themselves been discovered serendipitously. The mechanistic bases for their effectiveness have typically been elucidated post-hoc. At present, it is unclear which of many potential mechanisms reviewed in this supplement are relevant to the clinical effects of the KD. It would be far too difficult to integrate these numerous possibilities into a single unifying hypothesis (or a final common pathway), or to consider them simultaneously. Nevertheless, it might be instructive to consider each of these putative mechanisms one by one and ask a simple comparative question. If the mechanism or target in question is a critical determinant of the anticonvulsant efficacy of the KD, then would a similar intervention known to be based on that mechanism yield a comparable effect? Perhaps answering this question for each mechanistic speculation might help substantiate (or perhaps invalidate) that particular hypothesis.
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So is the clinical effectiveness of the KD simply a matter of increasing energy stores? If this is the case, then would it not be a simpler matter to ingest creatine, a highly bioavailable and relatively safe oral supplement, and one that is increasingly demonstrated to promote health and longevity (Beal, 2003; Bender et al., 2007; Schapira, 2008)?
The scientific rationale for elucidating mechanisms of disease pathogenesis or of therapeutic interventions has been traditionally based upon the lofty goal of discovering novel treatments, ones that would be more efficacious than existing options and also be devoid of side-effects altogether. Moreover, in epilepsy research, disease prevention or modification has become the “holy grail”, such that we are no longer complacent with symptomatic treatment and increasing attention is being given to understanding the processes of anti-epileptogenesis itself. Researchers in the field of the ketogenic diet (KD) have also embraced these tenets and recently embarked on that all-too-familiar Quixotic journey, with the ultimate aim of reducing the “difficult” KD regimen to a simple pill. If achieved, this result would represent an ironic recapitulation of the early history of the KD in the United States. Although the KD experienced an initial surge of interest following its introduction in the early 1920’s, it was relegated to near obscurity by the emergence of a familiar drug known as phenytoin. Henceforth, until the mid 1990’s, clinicians – for obvious practical reasons – found it simpler to prescribe a pill rather than an exacting diet.
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