While the evidence behind ketogenic diets for diabetes is still preliminary and the evidence for weight loss isn’t all that convincing (more on that next), the evidence of using the diet to treat epilepsy is extremely robust. The idea for treating people with epilepsy with the keto diet came about in the 1920s, when researchers observed that people who fasted experienced fewer seizures. (Researchers still aren’t sure why the diet can work for epilepsy, but a few mechanisms have been proposed, including making neurons more resilient during seizures.)
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Probably, and there are a few reasons why the keto diet usually equals weight-loss gold, says Keatley. For starters, people usually reduce their daily caloric intake to about 1,500 calories a day because healthy fats and lean proteins make you feel fuller sooner—and for a longer period of time. And then there’s the fact that it takes more energy to process and burn fat and protein than carbs, so you're burning slightly more calories than you did before. Over time, this can lead to weight loss.
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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.
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It usually takes three to four days for your body to go into ketosis because you have to use up your body's stores of glucose, i.e., sugar first, Keatley says. Any major diet change can give you some, uh, issues, and Keatley says he often sees patients who complain of IBS-like symptoms and feeling wiped out at the beginning of the diet. (The tiredness happens because you have less access to carbs, which give you quick energy, he explains.)
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The nerve impulse is characterised by a great influx of sodium ions through channels in the neuron's cell membrane followed by an efflux of potassium ions through other channels. The neuron is unable to fire again for a short time (known as the refractory period), which is mediated by another potassium channel. The flow through these ion channels is governed by a "gate" which is opened by either a voltage change or a chemical messenger known as a ligand (such as a neurotransmitter). These channels are another target for anticonvulsant drugs.
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Implementing the diet can present difficulties for caregivers and the patient due to the time commitment involved in measuring and planning meals. Since any unplanned eating can potentially break the nutritional balance required, some people find the discipline needed to maintain the diet challenging and unpleasant. Some people terminate the diet or switch to a less demanding diet, like the modified Atkins diet or the low-glycaemic index treatment diet, because they find the difficulties too great.
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The ketone bodies are possibly anticonvulsant; in animal models, acetoacetate and acetone protect against seizures. The ketogenic diet results in adaptive changes to brain energy metabolism that increase the energy reserves; ketone bodies are a more efficient fuel than glucose, and the number of mitochondria is increased. This may help the neurons to remain stable in the face of increased energy demand during a seizure, and may confer a neuroprotective effect.
Se puede tener convulsiones, pero un EEG normal,