Early studies reported high success rates; in one study in 1925, 60% of patients became seizure-free, and another 35% of patients had a 50% reduction in seizure frequency. These studies generally examined a cohort of patients recently treated by the physician (a retrospective study) and selected patients who had successfully maintained the dietary restrictions. However, these studies are difficult to compare to modern trials. One reason is that these older trials suffered from selection bias, as they excluded patients who were unable to start or maintain the diet and thereby selected from patients who would generate better results. In an attempt to control for this bias, modern study design prefers a prospective cohort (the patients in the study are chosen before therapy begins) in which the results are presented for all patients regardless of whether they started or completed the treatment (known as intent-to-treat analysis).
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.
In fact, patients with gastroesophageal reflux disease (GERD) have been shown to improve after eating very low carbohydrate diets.31, 32 Another study found increased carb-intake worsened GERD, while a high-fat, low-carbohydrate diet reduced symptoms.33 And two studies have linked esophageal diseases, including Barrett’s esophagus (BE)34 and GERD,35 to sugar and carbohydrate intake.
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Anticonvulsants suppress epileptic seizures, but they neither cure nor prevent the development of seizure susceptibility. The development of epilepsy (epileptogenesis) is a process that is poorly understood. A few anticonvulsants (valproate, levetiracetam and benzodiazepines) have shown antiepileptogenic properties in animal models of epileptogenesis. However, no anticonvulsant has ever achieved this in a clinical trial in humans. The ketogenic diet has been found to have antiepileptogenic properties in rats.
Cyclical keto diet: The Bulletproof Diet falls into this category. You eat high fat, low carb (less than 50 grams of net carbs a day) five to six days of the week. On day seven, you up your carb intake to roughly 150 grams, during what’s called a carb refeed day. Carb cycling this way helps you avoid the negative effects some people experience when they restrict carbs long term, like thyroid issues, fatigue and dry eyes. Learn more here about how carb cycling works.
Increases in cholesterol levels need discussion too. We do see temporary increases in cholesterol levels often as individuals transition onto a ketogenic diet. However, when you examine lipid particle size (a more important way to look at the cardiovascular risks), the risk pattern doesn’t seem to increase with a ketogenic diet. Harvard Health has written about lipid particle size here before: http://www.health.harvard.edu/womens-health/should-you-seek-advanced-cholesterol-testing-
On the ketogenic diet, carbohydrates are restricted and so cannot provide for all the metabolic needs of the body. Instead, fatty acids are used as the major source of fuel. These are used through fatty-acid oxidation in the cell's mitochondria (the energy-producing parts of the cell). Humans can convert some amino acids into glucose by a process called gluconeogenesis, but cannot do this by using fatty acids. Since amino acids are needed to make proteins, which are essential for growth and repair of body tissues, these cannot be used only to produce glucose. This could pose a problem for the brain, since it is normally fuelled solely by glucose, and most fatty acids do not cross the blood–brain barrier. However, the liver can use long-chain fatty acids to synthesise the three ketone bodies β-hydroxybutyrate, acetoacetate and acetone. These ketone bodies enter the brain and partially substitute for blood glucose as a source of energy.
When you’re eating the foods that get you there (more on that in a minute), your body can enter a state of ketosis in one to three days, she adds. During the diet, the majority of calories you consume come from fat, with a little protein and very little carbohydrates. Ketosis also happens if you eat a very low-calorie diet — think doctor-supervised, only when medically recommended diets of 600 to 800 total calories.