We are brazilian, living in Brazil. My daughter, Isabel, 21y. o., born in 1996, has syndrome of deficiency of Glut1. She was diagnosed around her first year of life. At that time her baby bottle, her begining diet meal, was 50ml water plus 50ml oil plus vitamin. Since then, which means, for 20 years, she is under this diet. For almost 18 years under 4:1 proportion. At this right moment 3:1. The only problem she had since started the diet were kidney stones in 2002. Nothing else. Grateful to the diet she doesn’t take any kind of medicine to avoid seizures. Her health is perfect, no colesterol at all. We are at your will for any issues related to her health.
Advocates for the diet recommend that it be seriously considered after two medications have failed, as the chance of other drugs succeeding is only 10%.[9][31][32] The diet can be considered earlier for some epilepsy and genetic syndromes where it has shown particular usefulness. These include Dravet syndrome, infantile spasms, myoclonic-astatic epilepsy, and tuberous sclerosis complex.[9][33]

The brain is composed of a network of neurons that transmit signals by propagating nerve impulses. The propagation of this impulse from one neuron to another is typically controlled by neurotransmitters, though there are also electrical pathways between some neurons. Neurotransmitters can inhibit impulse firing (primarily done by γ-aminobutyric acid, or GABA) or they can excite the neuron into firing (primarily done by glutamate). A neuron that releases inhibitory neurotransmitters from its terminals is called an inhibitory neuron, while one that releases excitatory neurotransmitters is an excitatory neuron. When the normal balance between inhibition and excitation is significantly disrupted in all or part of the brain, a seizure can occur. The GABA system is an important target for anticonvulsant drugs, since seizures may be discouraged by increasing GABA synthesis, decreasing its breakdown, or enhancing its effect on neurons.[7]
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]
Wilder's colleague, paediatrician Mynie Gustav Peterman, later formulated the classic diet, with a ratio of one gram of protein per kilogram of body weight in children, 10–15 g of carbohydrate per day, and the remainder of calories from fat. Peterman's work in the 1920s established the techniques for induction and maintenance of the diet. Peterman documented positive effects (improved alertness, behaviour, and sleep) and adverse effects (nausea and vomiting due to excess ketosis). The diet proved to be very successful in children: Peterman reported in 1925 that 95% of 37 young patients had improved seizure control on the diet and 60% became seizure-free. By 1930, the diet had also been studied in 100 teenagers and adults. Clifford Joseph Barborka, Sr., also from the Mayo Clinic, reported that 56% of those older patients improved on the diet and 12% became seizure-free. Although the adult results are similar to modern studies of children, they did not compare as well to contemporary studies. Barborka concluded that adults were least likely to benefit from the diet, and the use of the ketogenic diet in adults was not studied again until 1999.[10][14]
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]
My point here is that the warnings about the ketogenic principles are well taken and well documented. My concern is implications that this is a fad. I don’t use the word diet with my patients and I’m concerned that the principles behind the label and the real results that these readers have commented on might get minimized. I have found it best to encourage patients to read authors like: Stephen Phinney, Jeff Volek, Patricia Daly, and Charles Gant and the be partners with their doctors and check blood work as they move along. I am not for or against the article. If ketogenic principles offer people enduring, satisfying, and cohesive change then why not read about its potential and flexilbity?
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]
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A keto diet has shown to improve triglyceride levels and cholesterol levels most associated with arterial buildup. More specifically low-carb, high-fat diets show a dramatic increase in HDL and decrease in LDL particle concentration compared to low-fat diets.3A study in the long-term effects of a ketogenic diet shows a significant reduction in cholesterol levels, body weight, and blood glucose. Read more on keto and cholesterol >

Make things yourself. While it’s extremely convenient to buy most things pre-made or pre-cooked, it always adds to the price per pound on items. Try prepping veggies ahead of time instead of buying pre-cut ones. Try making your stew meat from a chuck roast. Or, simply try to make your mayo and salad dressings at home. The simplest of things can work to cut down on your overall grocery shopping.


Even low carb chips can contain inflammatory yeast or protein powders from grain-fed cows. This keto recipe gives you the same crunch and zesty flavor of cheesy store-bought chips without the harmful ingredients. Simply fry thin slices of zucchini then toss with spices for the perfect crunchy snack. Fry in heat-safe grass-fed ghee or beef tallow to make this recipe more Bulletproof.
Advocates for the diet recommend that it be seriously considered after two medications have failed, as the chance of other drugs succeeding is only 10%.[9][31][32] The diet can be considered earlier for some epilepsy and genetic syndromes where it has shown particular usefulness. These include Dravet syndrome, infantile spasms, myoclonic-astatic epilepsy, and tuberous sclerosis complex.[9][33]
The keto diet isn’t new, and it’s been around for nearly a century. It was originally developed to treat people with epilepsy. In the 1920s, researchers found that raised levels of ketones in the blood led to fewer epileptic seizures in patients. The keto diet is still used today to treat children with epilepsy who don’t respond well to anti-epileptic drugs.[2]
The ketone bodies are possibly anticonvulsant; in animal models, acetoacetate and acetone protect against seizures. The ketogenic diet results in adaptive changes to brain energy metabolism that increase the energy reserves; ketone bodies are a more efficient fuel than glucose, and the number of mitochondria is increased. This may help the neurons to remain stable in the face of increased energy demand during a seizure, and may confer a neuroprotective effect.[56]

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