The relevance of leptin to seizure susceptibility was recently highlighted by Erbayat-Altay and colleagues (2008) who demonstrated a significantly decreased threshold in leptin-deficient ob/ob mice to pentylenetetrazol-induced seizures. Indeed, leptin itself inhibits seizures induced by 4-aminopyridine and pentyelenetrazole-induced, possibly through blockade of AMPA receptor-mediated synaptic transmission (Xu et al., 2008). If the limiting of AMPA receptor-mediated transmission is a critical factor, it should be recalled this can also be accomplished by topiramate. With respect to the KD, the leptin signaling system is believed to contribute to slow weight gain associated with chronic treatment in both rodents and humans (Thio et al., 2006). KD-fed juvenile rodents had higher serum leptin levels and lower insulin levels than control rats fed a standard diet.

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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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