While the effects of leptin on seizure susceptibility and its relationship to KD-induced weight loss are intriguing, there are as yet no direct data supporting leptin as an anticonvulsant mediator of the KD. Certainly, the clinical implications of the study by Xu et al. (2008) are intriguing, namely, that intranasal administration of leptin might be efficacious in aborting acute seizure activity. And if the clinical effects of the KD are due in part to increased leptin levels, then accelerated development and validation of leptin as a novel anticonvulsant medication would be warranted.
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One of the nagging unresolved questions regarding ketone bodies is whether they correlate with seizure control. Recent studies have suggested that under certain conditions and in specific models, blood levels of ketones do not in fact correlate well with anticonvulsant effects (Hartman & Vining, 2007). However, ketone levels are known to vary considerably during the circadian cycle, mostly as a consequence of feeding schedules and subsequent metabolism of foodstuffs (DeGasquet et al., 1977). Despite numerous studies highlighting ketonemia following KD treatment, we still do not know what the true brain concentrations are, especially in the microenvironment of the highly metabolically active synapse. Moreover, there are other studies suggesting that high ketone body levels are not necessary for clinical efficacy of a high-fat diet against medically refractory epilepsies (Pfeifer & Thiele, 2005).

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In rats fed a KD, Ziegler et al (2003) found an increase in antioxidant activity using a luminol oxidation assay in the hippocampus, and a four-fold increase in glutathione peroxidase activity. Consistent with these findings, Jarrett et al (2008) recently reported an up-regulation of GSH biosynthesis in adolescent rats fed a KD. Furthermore, these investigators observed improved mitochondrial antioxidant status, and proposed that these changes were responsible for preventing mitochondrial DNA from oxidant-induced damage. Collectively, these studies suggest that the KD may indeed exert neuroprotective activity.

What investigators have elucidated over the past decade or so is that a variety of molecular, genetic, cellular, and metabolic factors are likely contributory to the clinical effects of the KD. As a generalization, it is becoming widely accepted that the mechanistic underpinnings of the KD are likely multiple, parallel, and possibly synergistic (Bough & Rho, 2007).

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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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