Ketogenic diet food

The ketogenic diet is very high in fats and low in carbohydrates. The ketogenic was first developed more than 80 years ago. It makes the body burn fat for energy instead of glucose. A ketogenic diet seizure is used to reduce the incidence of seizure. For general information on a healthy diet.

Ketogenic diet for Rett syndrome
Improvement of Motor and Exploratory Behavior in Rett Syndrome Mice with Restricted Ketogenic and Standard Diets.
Epilepsy Behav. 2009 Feb 25. Mantis JG, Fritz CL, Marsh J, Heinrichs SC, Seyfried TN. Biology Department, Boston College, Chestnut Hill, MA 02467.
Rett syndrome is a rare X-linked autistic-spectrum neurological disorder associated with impaired energy metabolism, seizure susceptibility, progressive social behavioral regression, and motor impairment primarily in young girls. The objective of this study was to examine the influence of restricted diets, including a ketogenic diet and a standard rodent chow diet (SD), on behavior in male Mecp2(308/y) mice, a model of rett syndrome. Restriction of either the ketogenic diet or the SD improved motor behavior and reduced anxiety. We conclude that although both restricted diets increased the tendency of Rett mice to explore a novel environment, the beneficial effects of the detogenic diet were due more to calorie restriction than to the composition of the diet. Our findings suggest that calorically restricted diets could be effective in reducing the anxiety and in improving motor behavior in girls with RTT.

ketogenic diet epilepsy research
Anticonvulsant mechanisms of the ketogenic diet.
Epilepsia. 2007 Jan;48(1):43-58. Bough KJ, Rho JM.Center for Drug Evaluation & Research, Food and Drug Administration, Rockville, Maryland.
The ketogenic diet is a broadly effective treatment for medically refractory epilepsy. Despite nearly a century of use, the mechanisms underlying its clinical efficacy remain unknown. In this review, we present one intersecting view of how the ketogenic diet may exert its anticonvulsant activity against the backdrop of several seemingly disparate mechanistic theories. We summarize key insights gleaned from experimental and clinical studies of the ketogenic diet, and focus particular attention on the role that ketone bodies, fatty acids, and limited glucose may play in seizure control. Chronic ketosis is anticipated to modify the tricarboxcylic acid cycle to increase GABA synthesis in brain, limit reactive oxygen species (ROS) generation, and boost energy production in brain tissue. Among several direct neuro-inhibitory actions, polyunsaturated fatty acids increased after ketogenic diet induce the expression of neuronal uncoupling proteins, a collective up-regulation of numerous energy metabolism genes, and mitochondrial biogenesis. These effects further limit ROS generation and increase energy production. As a result of limited glucose and enhanced oxidative phosphorylation, reduced glycolytic flux is hypothesized to activate metabolic K(ATP) channels and hyperpolarize neurons and/or glia. Although it is unlikely that a single mechanism, however well substantiated, will explain all of the diet's clinical benefits, these diverse, coordinated changes seem poised to stabilize synaptic function and increase the resistance to seizures throughout the brain.

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