This can look different for everybody, but some popular forms of this are the 16:8 diet, where you fast for 16 hours (usually from dinnertime until a late breakfast) and eat all your food within an eight-hour span. Another is the 5:2 diet, where you eat less than 500 calories for two non-consecutive days a week and then eat normally for the rest of the week.
Detrimentally, this results in high levels of both ketones and glucose. Extremely high ketone levels in the blood will elicit a dangerous biological environment that can even result in death. It must be clarified that DKA is very different than nutritional ketosis or fasting ketosis; ketone levels cannot be produced at such high levels in healthy individuals as they are with those in DKA.
The ketogenic diet is a mainstream dietary therapy that was developed to reproduce the success and remove the limitations of the non-mainstream use of fasting to treat epilepsy.[Note 2] Although popular in the 1920s and '30s, it was largely abandoned in favour of new anticonvulsant drugs.[1] Most individuals with epilepsy can successfully control their seizures with medication. However, 20–30% fail to achieve such control despite trying a number of different drugs.[9] For this group, and for children in particular, the diet has once again found a role in epilepsy management.[1][10]
“Your liver produces ketones all the time, but the rate depends on carbohydrate and protein intake,” says Jeff Volek, Ph.D., R.D., a professor of human sciences at Ohio State University. When the majority of your diet is made up of of carbs and protein, ketogenesis slows. Replacing carbs and protein with fat will put your body into ketosis, thus ramping up ketone production. Essentially, you're burning fat instead of carbs for energy. This process takes about three days to induce.
The ketogenic diet is a medical nutrition therapy that involves participants from various disciplines. Team members include a registered paediatric dietitian who coordinates the diet programme; a paediatric neurologist who is experienced in offering the ketogenic diet; and a registered nurse who is familiar with childhood epilepsy. Additional help may come from a medical social worker who works with the family and a pharmacist who can advise on the carbohydrate content of medicines. Lastly, the parents and other caregivers must be educated in many aspects of the diet for it to be safely implemented.[5]
Because the ketogenic diet alters the body's metabolism, it is a first-line therapy in children with certain congenital metabolic diseases such as pyruvate dehydrogenase (E1) deficiency and glucose transporter 1 deficiency syndrome,[35] which prevent the body from using carbohydrates as fuel, leading to a dependency on ketone bodies. The ketogenic diet is beneficial in treating the seizures and some other symptoms in these diseases and is an absolute indication.[36] However, it is absolutely contraindicated in the treatment of other diseases such as pyruvate carboxylase deficiency, porphyria, and other rare genetic disorders of fat metabolism.[9] Persons with a disorder of fatty acid oxidation are unable to metabolise fatty acids, which replace carbohydrates as the major energy source on the diet. On the ketogenic diet, their bodies would consume their own protein stores for fuel, leading to ketoacidosis, and eventually coma and death.[37]

If you’re looking to get a jump start on your health and fitness goals this year, you may be thinking about trying the ketogenic diet. Maybe you’ve heard the phrase before — it’s a huge diet buzzword — but aren’t sure what it means. Here’s a primer: The ketogenic diet is an eating plan that drives your body into ketosis, a state where the body uses fat as a primary fuel source (instead of carbohydrates), says Stacey Mattinson, RDN, who is based in Austin, Texas.


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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