The ketogenic diet achieved national media exposure in the US in October 1994, when NBC's Dateline television programme reported the case of Charlie Abrahams, son of Hollywood producer Jim Abrahams. The two-year-old suffered from epilepsy that had remained uncontrolled by mainstream and alternative therapies. Abrahams discovered a reference to the ketogenic diet in an epilepsy guide for parents and brought Charlie to John M. Freeman at Johns Hopkins Hospital, which had continued to offer the therapy. Under the diet, Charlie's epilepsy was rapidly controlled and his developmental progress resumed. This inspired Abrahams to create the Charlie Foundation to promote the diet and fund research.[10] A multicentre prospective study began in 1994, the results were presented to the American Epilepsy Society in 1996 and were published[17] in 1998. There followed an explosion of scientific interest in the diet. In 1997, Abrahams produced a TV movie, ...First Do No Harm, starring Meryl Streep, in which a young boy's intractable epilepsy is successfully treated by the ketogenic diet.[1]

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A keto diet has shown to improve triglyceride levels and cholesterol levels most associated with arterial buildup. More specifically low-carb, high-fat diets show a dramatic increase in HDL and decrease in LDL particle concentration compared to low-fat diets.3A study in the long-term effects of a ketogenic diet shows a significant reduction in cholesterol levels, body weight, and blood glucose. Read more on keto and cholesterol >

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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.[1] 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.[4][5]
Hi Fran, There could be many reasons and unfortunately the comment area is not the place for 1:1 support, but highly recommend our support group here for questions like this. The color on keto sticks does not indicate the amount of fat you are burning, only the amount of excess ketones that are spilling into urine combined with how dehydrated you are (or not). The goal is to be in ketosis, not necessarily a darker color.

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”According to the insulin-carbohydrate model, we should have seen an acceleration in the rate of body fat loss when insulin secretion was cut by 50 percent,” Hall told me when the study came out. But the researchers didn’t, which Hall thinks suggests that the regulation of fat tissue storage in the body has to do with more than just insulin levels and their relationship with the carbs we eat.

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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).[15] MCTs are more efficiently absorbed and are rapidly transported to the liver via the hepatic portal system rather than the lymphatic system.[16] 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.[15] The MCT diet replaced the classic ketogenic diet in many hospitals, though some devised diets that were a combination of the two.[10]

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In practice, that means subsisting mainly on meats, eggs, cheese, fish, nuts, butter, oils, and vegetables — and carefully avoiding sugar, bread and other grains, beans, and even fruit. Again, if this sounds familiar, it’s because it’s not that different from the Atkins diet, among the most famous very low-carb diets that promise to get your body burning fat. (Atkins, who reportedly said ketosis is “as delightful as sunshine and sex,” promised to help people “stay thin forever,” the same way the now popular Keto Reset Diet book promises to “burn fat forever.”)

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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.[7]

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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]

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