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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As mentioned above, this product uses a ketone called BHB. BHB is short for Beta-hydroxybutyrate, which your body makes naturally. It’s supposed to increase your energy and burn fat simultaneously. There are no studies, however, that verify these claims. Keto Pills attempt to simulate this process, but there is little evidence right now that corroborates these theories. There is some promising research for exogenous ketones. For example, this study concludes that exogenous ketone drinks effectively achieve ketosis. It should be mentioned that Keto Pills are not the same thing, so the comparison is a little unclear. Ketosis, by the way, is just a way of referring to the metabolic process of burning fat instead of carbohydrates for energy.
Alternatively, if simple calorie restriction is sufficient to prevent seizure activity in patients, why not decrease total caloric intake, and not bother with the high-fat KD? However, from yet another perspective, one could consider combining the KD and calorie restriction (as has been done in animal studies). In rats fed a calorie-restricted KD, Bough and colleagues (2003) demonstrated exhibited greater paired-pulse inhibition in the dentate gyrus, elevated maximal dentate activation threshold, and an absence of “spreading depression”-like events compared with ad libitum-fed controls. These results suggest that treatment with a calorie-restricted KD may produce both anticonvulsant and anti-epileptogenic effects.

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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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