We suggest that CR may underlie the anticonvulsant mechanism of the KD and that CR alone may be an effective antiepileptic diet therapy. Moreover, the anticonvulsant action of CR may operate through the combined effects of reducing blood glucose and elevating blood ketones, thereby modulating cerebral energy metabolism. Our preclinical findings in EL mice suggest that CR may be an effective dietary therapy for some human epilepsies because CR is easy to administer and is devoid of the adverse side effects associated with other antiepileptic therapies.
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