On the ketogenic diet, carbohydrates are restricted and so cannot provide for all the metabolic needs of the body. Instead, fatty acids are used as the major source of fuel. These are used through fatty-acid oxidation in the cell's mitochondria (the energy-producing parts of the cell). Humans can convert some amino acids into glucose by a process called gluconeogenesis, but cannot do this by using fatty acids.[57] Since amino acids are needed to make proteins, which are essential for growth and repair of body tissues, these cannot be used only to produce glucose. This could pose a problem for the brain, since it is normally fuelled solely by glucose, and most fatty acids do not cross the blood–brain barrier. However, the liver can use long-chain fatty acids to synthesise the three ketone bodies β-hydroxybutyrate, acetoacetate and acetone. These ketone bodies enter the brain and partially substitute for blood glucose as a source of energy.[56]
In pediatric patients whose seizures could not be treated with these anti-epileptic drugs, a ketogenic diet was able to reduce seizures by more than 50% in 54% of the young patients tested, with 10% of the cohort becoming seizure-free after one year on the diet.[28] Since this study, numerous additional studies have shown this modality to be effective for children and adults with epilepsy. Results of ketogenic diet–driven studies have included 55% of patients seeing a reduction in seizures by more than 50%,[29] and 27% of patients seeing a 90% or greater reduction in seizures with many entering into complete remission.[30]

Supplemental ketosis: This form of ketosis has recently gained momentum in the field of ketogenic dieting. Supplemental ketosis is a ketogenic state that is achieved through the ingestion of ketogenic supplements. Consuming these substances alone does not mean that an individual is “keto-adapted.” While these products can help during the keto-adaptation period, especially if one is experiencing the “keto-flu,” they will only elicit short-term increases in blood ketone levels. Exogenous ketones can acutely produce benefits similar to the ketogenic diet; however, these products are best used in conjunction with a well-formulated keto diet for beginners, or the very at least, a diet that restricts carbohydrates. The commonly used supplements on the market are medium-chain triglyceride (MCT) oil and exogenous ketones. MCT oil is a fat that, in contrast to other longer-chain fatty acids, travels straight from the intestines to the liver where it is readily metabolized. This allows for ketone production in the liver to occur faster than with other fats (long-chain fatty acids have to travel through the lymph and circulatory systems first). Exogenous ketones are synthetic substances that mimic the ketones produced in our body (endogenous ketones). Exogenous ketones can come in the form of ketone salts or ketone esters.


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]
How often you eat while on a keto diet plan is also up to your personal preference. "For most people, I recommend three to four meals per day with a few healthy keto snacks in between," says Dr. Axe. "This ensures that you're getting a good mix of protein and fat all day long to keep you feeling energized and satisfied." That being said, he encourages people to listen to their bodies and tune in to when they're truly hungry. "If you find that you feel better eating five to six smaller meals spread throughout the day, do what works best for you."

Cravings: As one begins to eliminate carbohydrates from the diet, it is common to experience carbohydrate cravings. Several suggestions for conquering these cravings are outlined below. However, it should be noted that as the body keto-adapts, hunger and appetite should become suppressed. One interesting study found that when you increase the occupied volume inside of the stomachs of subjects, this led to feelings of perceived fullness.[17] This means by doing things like drinking more water and eating more high volume foods we can improve our feeling of fullness.

A simple standby, but one that ketoers adore. 2 or 3 fried eggs and some bacon might not sound like much, but it’s full of protein that will keep you full and energized all morning. Take the opportunity on the weekend to lay your bacon strips on a single cookie sheet and bake in the oven for 20 minutes at 400 degrees. The result is the best bacon you’ve ever had, in a big batch, with no sitting over a popping, hissing frying pan.


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.[7]
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