Variations on the Johns Hopkins protocol are common. The initiation can be performed using outpatient clinics rather than requiring a stay in hospital. Often, no initial fast is used (fasting increases the risk of acidosis, hypoglycaemia, and weight loss). Rather than increasing meal sizes over the three-day initiation, some institutions maintain meal size, but alter the ketogenic ratio from 2:1 to 4:1.[9]
When dietary carbohydrate is broken down into the energy substrate glucose, thereby raising blood glucose levels, the pancreas is stimulated to secrete insulin (the hormone that stores fat and inhibits ketone production). However, when carbohydrate intake is restricted, insulin remains suppressed, and the body’s primary fuel source shifts from glucose to fat, priming the body to enter a state of ketosis. When fat oxidation/breakdown is increased to a certain extent, ketones are made in the liver through a process known as ketogenesis (i.e., keto + genesis = ketone formation). When carbohydrate intake is restricted, blood glucose and insulin levels decrease, which allows fat stores to be broken down rapidly for energy. Most cells in the body can utilize either fatty acids or ketones for fuel, including the brain, which has shown to be more efficient in the presence of ketones rather than glucose.
Rami co-founded Tasteaholics with Vicky at the start of 2015 to master the art of creating extremely delicious food while researching the truth behind nutrition, dieting and overall health. You can usually find him marketing, coding or coming up with the next crazy idea because he can’t sit still for too long. His favorite book is The 4-Hour Workweek and artist is Infected Mushroom.

The ketogenic diet is not a benign, holistic, or natural treatment for epilepsy; as with any serious medical therapy, complications may result.[28] These are generally less severe and less frequent than with anticonvulsant medication or surgery.[28] Common but easily treatable short-term side effects include constipation, low-grade acidosis, and hypoglycaemia if an initial fast is undertaken. Raised levels of lipids in the blood affect up to 60% of children[38] and cholesterol levels may increase by around 30%.[28] This can be treated by changes to the fat content of the diet, such as from saturated fats towards polyunsaturated fats, and if persistent, by lowering the ketogenic ratio.[38] Supplements are necessary to counter the dietary deficiency of many micronutrients.[18]
Keto for Parkinson’s Disease: Parkinson’s disease develops as a result of neuron death in the midbrain and is typically accompanied by tremors, as well as physical and cognitive impairments. Due to its neuroprotective effects, the ketogenic diet may help protect neurons, increase energy production and mitochondrial function, lower inflammation, and improve motor function—all of which play a role in Parkinson’s disease.

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]
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]
After initiation, the child regularly visits the hospital outpatient clinic where they are seen by the dietitian and neurologist, and various tests and examinations are performed. These are held every three months for the first year and then every six months thereafter. Infants under one year old are seen more frequently, with the initial visit held after just two to four weeks.[9] A period of minor adjustments is necessary to ensure consistent ketosis is maintained and to better adapt the meal plans to the patient. This fine-tuning is typically done over the telephone with the hospital dietitian[19] and includes changing the number of calories, altering the ketogenic ratio, or adding some MCT or coconut oils to a classic diet.[18] Urinary ketone levels are checked daily to detect whether ketosis has been achieved and to confirm that the patient is following the diet, though the level of ketones does not correlate with an anticonvulsant effect.[19] This is performed using ketone test strips containing nitroprusside, which change colour from buff-pink to maroon in the presence of acetoacetate (one of the three ketone bodies).[45]
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