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]
Electrolytes: To reiterate, maintaining electrolyte balances is critical on a ketogenic diet, in order to prevent side effects and the “keto-flu.” While this can be done exclusively through whole foods, some individuals may require additional sources. Sodium, magnesium, potassium, and in some cases, calcium, can all be replenished via supplementation.

2) Now you need to do a little learning before we move any further. Start by learning a bit more about ketosis itself, and the pitfalls you may experience. I love Bodybuilding.com and think that this article on the Keto Diet is perfect for beginners, so go check it out. Unless you are planning to start bodybuilding part, 2 of the post will not apply to you. 😉 

Keto-adaptation occurs as tissues maximally increase their capacity to utilize ketone bodies for fuel. As glucose metabolism slows and fatty acid breakdown ramps up, ketones are synthesized and increasingly utilized for fuel. After a few weeks or months of increasing ketone and fat utilization, the body adapts to these new fuel sources. In addition to increased fat breakdown and ketone synthesis and utilization, keto-adaptation is associated with decreased and stabilized blood glucose levels.
In most cases, the macronutrient profile for a keto diet for beginners consists of about 5–10% carbohydrates, 15–25% protein, and the remaining 65–80% from fat. By restricting glucogenic substrates (i.e. nutrients that increase blood glucose levels, like carbohydrates and glucogenic amino acids from proteins), a deeper level of ketosis can be achieved, which may have a plethora of benefits as discussed below. As an example, one study compared diets with 30, 60, and 100 grams of carbohydrates per day and found that restricting carbohydrates to 30 grams led to a greater increase in circulating ketone levels and body fat loss.[1]
Normal dietary fat contains mostly long-chain triglycerides (LCTs). Medium-chain triglycerides (MCTs) are more ketogenic than LCTs because they generate more ketones per unit of energy when metabolised. Their use allows for a diet with a lower proportion of fat and a greater proportion of protein and carbohydrate,[18] leading to more food choices and larger portion sizes.[4] The original MCT diet developed by Peter Huttenlocher in the 1970s derived 60% of its calories from MCT oil.[15] Consuming that quantity of MCT oil caused abdominal cramps, diarrhea, and vomiting in some children. A figure of 45% is regarded as a balance between achieving good ketosis and minimising gastrointestinal complaints. The classical and modified MCT ketogenic diets are equally effective and differences in tolerability are not statistically significant.[9] The MCT diet is less popular in the United States; MCT oil is more expensive than other dietary fats and is not covered by insurance companies.[18]
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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