Politi Keren, Shemer-Meiri Lilach, Shuper Avinoam, Aharoni S
Department of Pediatric and Adolescent Neurology, Schneider Children's Medical Center of Israel, Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Epilepsy Res Treat. 2011;2011:963637. doi: 10.1155/2011/963637. Epub 2011 Jun 5.
Although the ketogenic diet (KD) has been widely accepted as a legitimate and successful therapy for epilepsy and other neurological disorders, its mechanism of action remains an enigma. The use of the KD causes major metabolic changes. The most significant of them seems to be the situation of chronic ketosis, but there are others as well, for instance, high level of polyunsaturated fatty acids (PUFAs). These "primary" influences lead to "secondary", in part adaptive, effects, for instance changes in mitochondrial density and gene expression. Clinically, the influences of the diet are considered as anticonvulsive and neuroprotective, although neuroprotection can also lead to prevention of seizures. Potential clinical implications of these mechanisms are discussed.
尽管生酮饮食(KD)已被广泛认可为治疗癫痫和其他神经系统疾病的一种合理且成功的疗法,但其作用机制仍是个谜。采用生酮饮食会引起重大的代谢变化。其中最显著的似乎是慢性酮症状态,但也有其他变化,例如多不饱和脂肪酸(PUFAs)水平升高。这些“主要”影响会导致“次要”的、部分为适应性的效应,比如线粒体密度和基因表达的变化。在临床上,该饮食的影响被认为具有抗惊厥和神经保护作用,尽管神经保护也可导致癫痫发作的预防。本文讨论了这些机制的潜在临床意义。