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).
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The original therapeutic diet for paediatric epilepsy provides just enough protein for body growth and repair, and sufficient calories[Note 1] to maintain the correct weight for age and height. The classic therapeutic ketogenic diet was developed for treatment of paediatric epilepsy in the 1920s and was widely used into the next decade, but its popularity waned with the introduction of effective anticonvulsant medications. This classic ketogenic diet contains a 4:1 ratio by weight of fat to combined protein and carbohydrate. This is achieved by excluding high-carbohydrate foods such as starchy fruits and vegetables, bread, pasta, grains, and sugar, while increasing the consumption of foods high in fat such as nuts, cream, and butter. Most dietary fat is made of molecules called long-chain triglycerides (LCTs). However, medium-chain triglycerides (MCTs)—made from fatty acids with shorter carbon chains than LCTs—are more ketogenic. A variant of the classic diet known as the MCT ketogenic diet uses a form of coconut oil, which is rich in MCTs, to provide around half the calories. As less overall fat is needed in this variant of the diet, a greater proportion of carbohydrate and protein can be consumed, allowing a greater variety of food choices.
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This is a delicious collection of recipes for breakfasts, lunches, dinners, sweet and savory snacks, drinks, and extra-fatty sauces. The recipes are packed with handy extras that make them even easier to use and adapt, from portion sizes to comprehensive nutrition information to substitutions for those with dietary restrictions, such as vegetarians and people with food allergies.
For example, if we told you to eat 50 total carbs rather than 20-30 grams of net carbs, you could be eating anywhere between 0 and 50 grams of net carbs. At 0 grams of net carbs, most people will get into ketosis within the first week and experience deeper levels of ketosis as the weeks progress. On the other hand, while eating 50 grams of net carbs per day, many people will struggle to get into ketosis and sustain higher ketone levels.
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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First reported in 2003, the idea of using a form of the Atkins diet to treat epilepsy came about after parents and patients discovered that the induction phase of the Atkins diet controlled seizures. The ketogenic diet team at Johns Hopkins Hospital modified the Atkins diet by removing the aim of achieving weight loss, extending the induction phase indefinitely, and specifically encouraging fat consumption. Compared with the ketogenic diet, the modified Atkins diet (MAD) places no limit on calories or protein, and the lower overall ketogenic ratio (about 1:1) does not need to be consistently maintained by all meals of the day. The MAD does not begin with a fast or with a stay in hospital and requires less dietitian support than the ketogenic diet. Carbohydrates are initially limited to 10 g per day in children or 20 g per day in adults, and are increased to 20–30 g per day after a month or so, depending on the effect on seizure control or tolerance of the restrictions. Like the ketogenic diet, the MAD requires vitamin and mineral supplements and children are carefully and periodically monitored at outpatient clinics.
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When you approach your normal body weight, the weight loss will slow. Just remember, a “normal” body weight differs from person to person depending on our genetics and environmental exposures and may not fit what we see in the popular media. The weight loss won’t go on forever. As long as you follow the advice to eat when you are hungry, you will eventually stabilize your weight.
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In the first month of the study, participants were put on a baseline diet, which was designed to be similar to what they reported they were eating outside the hospital, including lots of sugary carbohydrates. For the second month, the participants got the same amount of calories and protein as they did in the first month of the study, but ramped up the amount of fat in their food and ate far fewer carbs.
The day before admission to hospital, the proportion of carbohydrate in the diet may be decreased and the patient begins fasting after his or her evening meal. On admission, only calorie- and caffeine-free fluids are allowed until dinner, which consists of "eggnog"[Note 8] restricted to one-third of the typical calories for a meal. The following breakfast and lunch are similar, and on the second day, the "eggnog" dinner is increased to two-thirds of a typical meal's caloric content. By the third day, dinner contains the full calorie quota and is a standard ketogenic meal (not "eggnog"). After a ketogenic breakfast on the fourth day, the patient is discharged. Where possible, the patient's current medicines are changed to carbohydrate-free formulations.
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Adequate protein intake and developing ketosis are both critical for maximising fat loss and sparing muscle mass during the ketogenic diet. However, it will take up to 3 weeks before your body gets keto-adapted (in some cases even more). During the initial phase of the ketogenic diet, nitrogen losses may occur if your daily net carbs intake is very low. When your carbohydrate intake goes down, your body converts body protein into glucose. Since about 16% of protein is nitrogen, you may lose muscle mass which will cause a decrease in your metabolic rate. This could have a negative impact on fat loss. For example, if your carbs intake is close to zero, you you may have to eat more protein (aka protein sparing modified fast). Keep in mind this applies to zero carbohydrate intake which means it does not affect most people following the ketogenic diet.
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This content is strictly the opinion of Dr. Josh Axe and is for informational and educational purposes only. It is not intended to provide medical advice or to take the place of medical advice or treatment from a personal physician. All readers/viewers of this content are advised to consult their doctors or qualified health professionals regarding specific health questions. Neither Dr. Axe nor the publisher of this content takes responsibility for possible health consequences of any person or persons reading or following the information in this educational content. All viewers of this content, especially those taking prescription or over-the-counter medications, should consult their physicians before beginning any nutrition, supplement or lifestyle program.
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Achieving ketosis is a pretty straightforward, but it can seem complicated and confusing with all of the information out there.4If you want to learn more about ketosis and the scientific process around it, you can visit a very in-depth discussion about on Dr. Peter Attia’s website. Here’s the bottom line on what you need to do, ordered in levels of importance:
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During the 1920s and 1930s, when the only anticonvulsant drugs were the sedative bromides (discovered 1857) and phenobarbital (1912), the ketogenic diet was widely used and studied. This changed in 1938 when H. Houston Merritt, Jr. and Tracy Putnam discovered phenytoin (Dilantin), and the focus of research shifted to discovering new drugs. With the introduction of sodium valproate in the 1970s, drugs were available to neurologists that were effective across a broad range of epileptic syndromes and seizure types. The use of the ketogenic diet, by this time restricted to difficult cases such as Lennox–Gastaut syndrome, declined further.
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