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Over the past decade, much progress has been made in dissecting apart the mechanisms underlying the anticonvulsant (and potentially, neuroprotective) effects of the KD (Gasior et al., 2006; Bough & Rho, 2007). The complex systemic and metabolic changes induced by a high-fat, low-carbohydrate diet – not surprisingly – provide fertile ground for very innovative and speculative hypotheses linking certain adaptations to a net anticonvulsant effect, ones that by necessity take researchers back to the earlier days of introductory biochemistry and human physiology. While many intriguing concepts and research data have been reviewed systematically in the context of the international symposium from which this supplement stems, the fundamental question of how the KD works remains as tantalizing as ever.
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Polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA, C22: 6ω-3), arachidonic acid (AA, C20: 4ω-3), or eicosapentaenoic acid (EPA, C20: 5ω-3) have been reported to suppress voltage-gated sodium channels and L-type calcium channels in seizure-prone structures such as the hippocampus (Vreugdenhil et al., 1996). The KD produces elevations of both AA and DHA in serum (Fraser et al., 2003; Cunnane et al., 2002) and brain (Taha et al., 2005) of patients and animals, respectively, suggesting that these substrates might exert anticonvulsant effects by inhibiting sodium and calcium channels, like many anticonvulsant drugs (Xiao et al., 1997, 1998).
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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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Given these observations, would it be practical to package acetoacetate or acetone into a pill? While ketone bodies in situ are likely to influence local cellular bioenergetics, there are profound logistical constraints precluding ease of administration in humans to achieve comparable low millimolar concentrations observed in clinical practice (Hartman & Vining, 2007). Acetoacetate is highly unstable, as it has an immediate tendency to spontaneously decarboxylate, and acetone is a well known solvent that can cause significant mucosal irritation. Finally, oral ingestion of β-hydroxybutyrate formulations to achieve such concentrations may not be readily achievable (Smith et al., 2005). These considerations pose not insignificant challenges toward the design of a ketone pill.
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