Keto is often suggested for children who suffer from certain disorders (like Lennox-Gastaut syndrome or Rett syndrome) and don’t respond to seizure medication, according to the Epilepsy Foundation. (1) They note that keto can decrease the number of seizures these children have by half, with 10 to 15 percent becoming seizure-free. In other cases, it may also help patients reduce the dose of their medication.
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In the 1960s, medium-chain triglycerides (MCTs) were found to produce more ketone bodies per unit of energy than normal dietary fats (which are mostly long-chain triglycerides). MCTs are more efficiently absorbed and are rapidly transported to the liver via the hepatic portal system rather than the lymphatic system. The severe carbohydrate restrictions of the classic ketogenic diet made it difficult for parents to produce palatable meals that their children would tolerate. In 1971, Peter Huttenlocher devised a ketogenic diet where about 60% of the calories came from the MCT oil, and this allowed more protein and up to three times as much carbohydrate as the classic ketogenic diet. The oil was mixed with at least twice its volume of skimmed milk, chilled, and sipped during the meal or incorporated into food. He tested it on 12 children and adolescents with intractable seizures. Most children improved in both seizure control and alertness, results that were similar to the classic ketogenic diet. Gastrointestinal upset was a problem, which led one patient to abandon the diet, but meals were easier to prepare and better accepted by the children. The MCT diet replaced the classic ketogenic diet in many hospitals, though some devised diets that were a combination of the two.
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In 1921, Rollin Turner Woodyatt reviewed the research on diet and diabetes. He reported that three water-soluble compounds, β-hydroxybutyrate, acetoacetate, and acetone (known collectively as ketone bodies), were produced by the liver in otherwise healthy people when they were starved or if they consumed a very low-carbohydrate, high-fat diet. Dr. Russell Morse Wilder, at the Mayo Clinic, built on this research and coined the term "ketogenic diet" to describe a diet that produced a high level of ketone bodies in the blood (ketonemia) through an excess of fat and lack of carbohydrate. Wilder hoped to obtain the benefits of fasting in a dietary therapy that could be maintained indefinitely. His trial on a few epilepsy patients in 1921 was the first use of the ketogenic diet as a treatment for epilepsy.
The ketogenic diet has been studied in at least 14 rodent animal models of seizures. It is protective in many of these models and has a different protection profile than any known anticonvulsant. Conversely, fenofibrate, not used clinically as an antiepileptic, exhibits experimental anticonvulsant properties in adult rats comparable to the ketogenic diet. This, together with studies showing its efficacy in patients who have failed to achieve seizure control on half a dozen drugs, suggests a unique mechanism of action.
Parkinson’s Disease Because these patients are at a higher risk for dementia, researchers like Robert Krikorian, PhD, professor of clinical psychiatry and the director of the division of psychology at the University of Cincinnati College of Medicine in Ohio, are studying how inducing nutritional ketosis may be used to preserve cognitive functioning.
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After about two to seven days of following the keto diet, you go into something called ketosis, or the state your body enters when it doesn't have enough carbs for your cells to use for energy. That's when you start making ketones, or organic compounds that your bod then uses in place of those missing carbs. At this point, your body also starts burning fat for more energy, says Beth Warren, R.D., founder of Beth Warren Nutrition and author of Living A Real Life With Real Food.