Epilepsy & Developmental Disabilities

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Epilepsy & Developmental Disabilities

Beyond weight-loss, perhaps the most widely-known benefit of the ketogenic diet is the suppression of seizures and seizure-like activity. Originally founded in the 1920s at the Mayo Clinic, the ketogenic diet was conceived as a nutritional therapy by a physician named Dr. Russell Wilder. Carbohydrate reduction was proposed as a way to mimic fasting and induce ketonemia (increased ketone levels). This idea translated into a high-fat, moderate protein, low carbohydrate diet with a significant impact on seizure activity. Wilder reported that out of over 1,000 pediatric patients, 52% of these individuals had complete control, while 27% has improved control over their seizure activity. While the exact mechanism of action is still not fully understood, some theories include changes in neurotransmitter levels, improved energy production, modification to the TCA cycle, and reduced reactive oxygen species. The leading theory suggests the ketogenic diet promotes hyperpolarization. Like most processes within your body, neural signals are carried out based on changes in ion distribution. Ions are charged molecules and changes in a membrane’s charge are what trigger an action potential, which is just an impulse that travels down a neuron and causes the release of neurotransmitters. These neurotransmitters are the signaling molecules of the brain. While different neurotransmitters have different functions, one thing remains the same– your body requires them to be in balance in order to function properly. Too many excitatory neurotransmitters can lead to seizures, while too few may lead to psychiatric disorders. Glutamate is the primary excitatory neurotransmitter, while GABA is the primary inhibitory. A well-known cause of seizures is high levels of glutamate which causes increased excitation and thus seizures. The ketogenic diet helps balance and stabilize levels by promoting a glutamate-to-GABA shift, meaning it increases the chemicals needed to convert the glutamate to GABA. This balance promotes homeostasis through a reduction in excitation.

Furthermore, because carbohydrate reduction leads to the production of ketone bodies, the brain is provided with an alternative fuel source. Ketones do not require the same transporters as glucose, rather they use M.C.T.’s or Monocarboxylic Transporters (not to be confused with Medium Chain Triglycerides). The alternative transporter coupled with the size and polarity of ketone bodies, allow for them to rapidly cross the blood-brain barrier and provide energy to the brain, even when glucose transportation is limited– as is the case of certain neurological diseases.


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The Neuropharmacology of the Ketogenic Diet

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The Anticonvulsant Effects of Ketogenic Diet on Epileptic Seizures and Potential Mechanisms

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