Abstract :The Ketogenic Diet (KD) represents a well-known therapeutic option for refractory epilepsy
[1], although mechanisms regulating its anticonvulsant effects still remain partially unknown [2].
Human brain derives over 60% of its energy from ketones when glucose availability is limited.
After prolonged periods of fasting or during a KD, the whole body utilizes energy obtained
from Free Fatty Acids (FFAs) released from adipose tissue. However, the brain is not capable to
obtain significant energy from FFAs, thus hepatic ketogenesis converts them into ketone bodies:
ß-hydroxybutyrate (BHB) and Acetoacetate (AcAc), while a percentage of AcAc spontaneously
decarboxylates to acetone [3]. Recent perspectives about the KD potentials and neuro protective
properties strongly support its experimental and clinical application in a wide plethora of different
neurological diseases [4]. Notably, the metabolic state of mild ketosis, induced through KD
administration, calorie restriction or fasting, may be used to metabolically manage epilepsy and
a number neurodegenerative syndromes [5], amyotrophic lateral sclerosis [6], and some types of
cancer [7,8].