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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Given these findings, it is not surprising that investigators have studied the effects of dietary supplementation with PUFAs alone, to determine whether these substrates can render an anticonvulsant effect. Early case reports suggested that seizures might be better controlled with this approach (Schlanger et al., 2002). However, a recent randomized trial in adult patients with epilepsy failed to demonstrate superiority of a PUFA supplement (EPA) plus DHA, 2.2 mg/day in a 3:2 ratio) over placebo (Bromfield et al., 2008). Thus, the jury is still out as to whether PUFAs alone can mirror the clinical effects of the KD.

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