A study with an intent-to-treat prospective design was published in 1998 by a team from the Johns Hopkins Hospital and followed-up by a report published in 2001. 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.
At the start of a keto diet for beginners, it is not uncommon for an individual to experience rapid weight loss. This may concern some people, but it is worth noting that not ALL weight lost is body fat. When we lower our carbohydrate intake our insulin lowers, causing us to excrete more water. Additionally, reducing carbohydrate intake causes the body to break down glycogen stores (to initially maintain blood sugar levels); glycogen is the storage form of glucose that is located in our liver and skeletal muscle. The loss of both water and glycogen accounts for most of the weight loss in the first few days. Don’t be discouraged! Soon after, total body water and glycogen levels will balance out.
There are so many tricks, shortcuts, and gimmicks out there on achieving optimal ketosis – I’d suggest you don’t bother with any of that. Optimal ketosis can be accomplished through dietary nutrition alone (aka just eating food). You shouldn’t need a magic pill to do it. Just stay strict, remain vigilant, and be focused on recording what you eat (to make sure your carb and protein intake are correct).
Just because you're not eating all your fave carb-y foods, that doesn't mean you're going to go hungry. You'll be loading up on healthy fats (like olive oil and avocado), along with plenty of lean protein like grass-fed beef and chicken, and leafy greens or other non-starchy veggies. (Check out this printable keto diet grocery list, plus this additional comprehensive list of keto foods recommended by nutritionists, to get started.)
Physicians of ancient Greece treated diseases, including epilepsy, by altering their patients' diet. An early treatise in the Hippocratic Corpus, On the Sacred Disease, covers the disease; it dates from c. 400 BC. Its author argued against the prevailing view that epilepsy was supernatural in origin and cure, and proposed that dietary therapy had a rational and physical basis.[Note 3] In the same collection, the author of Epidemics describes the case of a man whose epilepsy is cured as quickly as it had appeared, through complete abstinence of food and drink.[Note 4] The royal physician Erasistratus declared, "One inclining to epilepsy should be made to fast without mercy and be put on short rations."[Note 5] Galen believed an "attenuating diet"[Note 6] might afford a cure in mild cases and be helpful in others.
There are many ways in which epilepsy occurs. Examples of pathological physiology include: unusual excitatory connections within the neuronal network of the brain; abnormal neuron structure leading to altered current flow; decreased inhibitory neurotransmitter synthesis; ineffective receptors for inhibitory neurotransmitters; insufficient breakdown of excitatory neurotransmitters leading to excess; immature synapse development; and impaired function of ionic channels.