Advocates for the diet recommend that it be seriously considered after two medications have failed, as the chance of other drugs succeeding is only 10%.[9][31][32] The diet can be considered earlier for some epilepsy and genetic syndromes where it has shown particular usefulness. These include Dravet syndrome, infantile spasms, myoclonic-astatic epilepsy, and tuberous sclerosis complex.[9][33]
Other big studies comparing popular diets of different macronutrient compositions, like the one I mentioned above, consistently suggest that the very low-carb approach isn’t a sustainable solution for weight loss. A review of the research on weight loss for different types of diets, published in the Lancet in 2015, found that people on low-carb diets lost 1 kilogram of additional weight after one year compared to people on low-fat diets — again, a marginal difference.
A study with an intent-to-treat prospective design was published in 1998 by a team from the Johns Hopkins Hospital[20] and followed-up by a report published in 2001.[21] As with most studies of the ketogenic diet, no control group (patients who did not receive the treatment) was used. The study enrolled 150 children. After three months, 83% of them were still on the diet, 26% had experienced a good reduction in seizures, 31% had had an excellent reduction, and 3% were seizure-free.[Note 7] At 12 months, 55% were still on the diet, 23% had a good response, 20% had an excellent response, and 7% were seizure-free. Those who had discontinued the diet by this stage did so because it was ineffective, too restrictive, or due to illness, and most of those who remained were benefiting from it. The percentage of those still on the diet at two, three, and four years was 39%, 20%, and 12%, respectively. During this period, the most common reason for discontinuing the diet was because the children had become seizure-free or significantly better. At four years, 16% of the original 150 children had a good reduction in seizure frequency, 14% had an excellent reduction, and 13% were seizure-free, though these figures include many who were no longer on the diet. Those remaining on the diet after this duration were typically not seizure-free, but had had an excellent response.[21][22]

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The benefits for the participants following the very low-carb diets weren’t nearly as dramatic as keto proponents claim. While the participants saw their insulin levels drop and stay low, they only saw a small increase in calorie burn, and that waned over time. (That short-lived increase in calorie burn amounted to about 100 extra calories per day — much less than the 400 to 600 calories promised by low-carb gurus.)

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The ketogenic diet is a high-fat, adequate-protein, low-carbohydrate diet that in medicine is used primarily to treat difficult-to-control (refractory) epilepsy in children. The diet forces the body to burn fats rather than carbohydrates. Normally, the carbohydrates contained in food are converted into glucose, which is then transported around the body and is particularly important in fueling brain function. However, if little carbohydrate remains in the diet, the liver converts fat into fatty acids and ketone bodies. The ketone bodies pass into the brain and replace glucose as an energy source. An elevated level of ketone bodies in the blood, a state known as ketosis, leads to a reduction in the frequency of epileptic seizures.[1] Around half of children and young people with epilepsy who have tried some form of this diet saw the number of seizures drop by at least half, and the effect persists even after discontinuing the diet.[2] Some evidence indicates that adults with epilepsy may benefit from the diet, and that a less strict regimen, such as a modified Atkins diet, is similarly effective.[1] Potential side effects may include constipation, high cholesterol, growth slowing, acidosis, and kidney stones.[3]

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Con: Results can vary depending on how much fluid you drink. By drinking more water, you dilute the concentration of ketones in the urine and thus a lower level of ketones will be detected on the strips. The strips don’t show a precise ketone level. Finally, and most importantly, as you become increasingly keto-adapted and your body reabsorbs ketones from the urine, urine strips may become unreliable, even if you’re in ketosis.
Over 8–10 mmol/l: It’s normally impossible to get to this level just by eating a keto diet. It means that something is wrong. The most common cause by far is type 1 diabetes, with severe lack of insulin. Symptoms include feeling very sick with nausea, vomiting, abdominal pain and confusion. The possible end result, ketoacidosis, may be fatal and requires immediate medical care. Learn more

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But people who started following the keto diet noticed weight loss for a few reasons: When you eat carbs, your body retains fluid in order to store carbs for energy (you know, in case it needs it). But when you’re not having much in the carb department, you lose this water weight, says Warren. Also, it's easy to go overboard on carbohydrates—but if you're loading up on fat, it may help curb cravings since it keeps you satisfied.

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Conklin's fasting therapy was adopted by neurologists in mainstream practice. In 1916, a Dr McMurray wrote to the New York Medical Journal claiming to have successfully treated epilepsy patients with a fast, followed by a starch- and sugar-free diet, since 1912. In 1921, prominent endocrinologist Henry Rawle Geyelin reported his experiences to the American Medical Association convention. He had seen Conklin's success first-hand and had attempted to reproduce the results in 36 of his own patients. He achieved similar results despite only having studied the patients for a short time. Further studies in the 1920s indicated that seizures generally returned after the fast. Charles P. Howland, the parent of one of Conklin's successful patients and a wealthy New York corporate lawyer, gave his brother John Elias Howland a gift of $5,000 to study "the ketosis of starvation". As professor of paediatrics at Johns Hopkins Hospital, John E. Howland used the money to fund research undertaken by neurologist Stanley Cobb and his assistant William G. Lennox.[10]

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