This episode explores the use and effectiveness of a ketogenic diet for controlling seizures in refractory epilepsy. It discusses the origins and effectiveness of the diet, the potential anti-convulsant properties of acetone, and the historical use of dietary therapy for epilepsy.
The ketogenic diet can effectively control seizures in refractory epilepsy by inducing a ketotic state through high-fat, low-carbohydrate intake.
The mechanisms behind the effectiveness of the ketogenic diet in reducing seizures include the GABA shunt, metabolic changes, and the presence of acetone, but further research is needed.
Deep dives
The Origins of the Ketogenic Diet for Epilepsy
The ketogenic diet for epilepsy originated in the early 1920s when a physician named Hugh Conklin theorized that epilepsy could be cured by starving patients. This led to a study where children with epilepsy were starved for up to 25 days, resulting in a reduction in seizures. Later, physician Russell Wilder discovered that it was the ketotic state induced by starvation, not the starvation itself, that controlled epilepsy. He then developed a high-fat, low-carbohydrate diet known as the ketogenic diet, which was found to be just as effective as starvation in reducing seizure burden.
Clinical Evidence and Efficacy of the Ketogenic Diet
Clinical trials have shown the efficacy of the ketogenic diet in reducing seizure burden, particularly in children with epilepsy. A 1924 study at the Mayo Clinic treated 17 epileptic patients with the ketogenic diet, of which 10 became seizure-free. Subsequent studies and a 2020 Cochrane review have confirmed the effectiveness of the diet in reducing seizures in children with epilepsy. Although there are now better medical options available, the ketogenic diet is still used in cases of refractory epilepsy where traditional anticonvulsant therapy is unsuccessful.
Mechanisms of the Ketogenic Diet in Epilepsy
The mechanisms behind the effectiveness of the ketogenic diet in controlling seizures are not fully understood, but several hypotheses have been proposed. One theory involves the GABA shunt, where ketones are converted into glutamate and then GABA, an inhibitory neurotransmitter that suppresses seizures. Another hypothesis is the metabolic hypothesis, which suggests that decreasing glucose-based metabolism in the brain has anticonvulsant effects. Animal studies have shown that inhibiting glycolysis, the process that utilizes glucose for energy, can protect against seizures. Additionally, the presence of acetone, a type of ketone, in the blood and its ability to cross the blood-brain barrier have been linked to anti-convulsant properties. However, further research is needed to fully understand these mechanisms.