There is nothing inherently difficult about following a ketogenic diet. We have many patients who do this very easily over many years. The metabolic benefits significantly outway any perceived challenges from limiting particular food types. Uptake would be far more widespread if nutrition professionals left their predujical opinions of SFA’s behind. Finally, given the expertise in Ketogenic Diets at Harvard, Dr David Ludwig, for one springs to mind, I am surprised the author did not avail themselves of the local expertise.
^ Freeman JM, Vining EP, Pillas DJ, Pyzik PL, Casey JC, Kelly LM. The efficacy of the ketogenic diet—1998: a prospective evaluation of intervention in 150 children. Pediatrics. 1998 Dec;102(6):1358–63. doi:10.1542/peds.102.6.1358. PMID 9832569. https://web.archive.org/web/20040629224858/http://www.hopkinsmedicine.org/press/1998/DECEMBER/981207.HTM Lay summary]—JHMI Office of Communications and Public Affairs. Updated 7 December 1998. Cited 6 March 2008.
The first modern study of fasting as a treatment for epilepsy was in France in 1911. Twenty epilepsy patients of all ages were "detoxified" by consuming a low-calorie vegetarian diet, combined with periods of fasting and purging. Two benefited enormously, but most failed to maintain compliance with the imposed restrictions. The diet improved the patients' mental capabilities, in contrast to their medication, potassium bromide, which dulled the mind.
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.
The low glycaemic index treatment (LGIT) is an attempt to achieve the stable blood glucose levels seen in children on the classic ketogenic diet while using a much less restrictive regimen. The hypothesis is that stable blood glucose may be one of the mechanisms of action involved in the ketogenic diet, which occurs because the absorption of the limited carbohydrates is slowed by the high fat content. Although it is also a high-fat diet (with approximately 60% calories from fat), the LGIT allows more carbohydrate than either the classic ketogenic diet or the modified Atkins diet, approximately 40–60 g per day. However, the types of carbohydrates consumed are restricted to those that have a glycaemic index lower than 50. Like the modified Atkins diet, the LGIT is initiated and maintained at outpatient clinics and does not require precise weighing of food or intensive dietitian support. Both are offered at most centres that run ketogenic diet programmes, and in some centres they are often the primary dietary therapy for adolescents.
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.
You may spot low-carb and sugar-free ice cream in your grocery store’s freezer case. Take one look at the ingredients, though, and you’ll find artificial colors, potentially moldy corn products, and sucralose that can harm your gut bacteria. This version tastes like a dirty keto recipe, but sweetens the results with grass-fed butter, collagen protein, and simple flavors like cocoa powder and cinnamon.
So rather than giving one-size-fits-all dietary advice or weaponizing the word “balanced” it might be better if the medical community suggested that there are Individual differences that need to be considered. This might also help those lay folk who have had success with one dietary lifestyle or another also realize that what’s valid for them may not be good advice for others.
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In 1921, Rollin Turner Woodyatt reviewed the research on diet and diabetes. He reported that three water-soluble compounds, β-hydroxybutyrate, acetoacetate, and acetone (known collectively as ketone bodies), were produced by the liver in otherwise healthy people when they were starved or if they consumed a very low-carbohydrate, high-fat diet. Dr. Russell Morse Wilder, at the Mayo Clinic, built on this research and coined the term "ketogenic diet" to describe a diet that produced a high level of ketone bodies in the blood (ketonemia) through an excess of fat and lack of carbohydrate. Wilder hoped to obtain the benefits of fasting in a dietary therapy that could be maintained indefinitely. His trial on a few epilepsy patients in 1921 was the first use of the ketogenic diet as a treatment for epilepsy.
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.
Furthermore, humans develop a condition dubbed ‘rabbit starvation’ when they eat a diet that is low in fat and carbohydrates, and high in protein (> 35% of total daily energy intake). This is due to the inability of the human liver to sufficiently upregulate urea synthesis to meet excessive loads of protein. Consequently, hyperaminoacidemia, hyperammonemia, hyperinsulinemia, nausea, diarrhea, and even death can ensue within 2 to 3 weeks. These effects were recognized historically through the excess consumption of lean wild meat by early American explorers.
I was a Corpsman (not a corpse-man as some recent somewhat fanatical president would say), and I can tell you many stories of Marines and Sailors who maintained restrictive diets (aka picky eaters). Most obvious was lack of sustaining energy (hypoglycemia) at mile 15 (with 80lbs of gear including a 6.5lb rifle and 200 rnds of ammo, etc.) and depletion of essential vitamins, electrolyte imbalance. They were always the first to collapse and have to hear me scold “see I told you so.” An IV of D5W usually does the trick (D is for dextrose, OMG!)
The final one is the area that I and many others who have pursued a state of ketosis fall into. At this point in my life, I have no chronic diseases, I feel great 99% of the time, but I am always looking to improve my productivity and performance. I have found being in mild-ketosis to be one of the best ways to improve my energy, mental acuity, creativity, physical strength and overall life performance.
Although excellent sources of fat, nuts add up quickly in protein and carbs, and are often inflammatory. Snack on fattier nuts such as macadamia nuts and pecans, but limit those high in inflammatory omega-6s, like peanuts and sunflower seeds. Only use nut flours (almond, coconut) in moderation, as they are packed with protein. To stay in ketosis, limit high-carb nuts like cashews, pistachios and chestnuts, and avoid most beans.
Children who discontinue the diet after achieving seizure freedom have about a 20% risk of seizures returning. The length of time until recurrence is highly variable, but averages two years. This risk of recurrence compares with 10% for resective surgery (where part of the brain is removed) and 30–50% for anticonvulsant therapy. Of those who have a recurrence, just over half can regain freedom from seizures either with anticonvulsants or by returning to the ketogenic diet. Recurrence is more likely if, despite seizure freedom, an electroencephalogram shows epileptiform spikes, which indicate epileptic activity in the brain but are below the level that will cause a seizure. Recurrence is also likely if an MRI scan shows focal abnormalities (for example, as in children with tuberous sclerosis). Such children may remain on the diet longer than average, and children with tuberous sclerosis who achieve seizure freedom could remain on the ketogenic diet indefinitely.
A: The amount of weight you lose is entirely dependent on you. Obviously adding exercise to your regimen will speed up your weight loss. Cutting out things that are common “stall” causes is also a good thing. Artificial sweeteners, dairy, wheat products and by-products (wheat gluten, wheat flours, and anything with an identifiable wheat product in it).
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.
My kidney doctor said that he has never seen anything like that before and wanted to know what I was doing. I told him that I was doing a combination of a ketogenic diet and daily coffee enemas through the training I got in your Keto and Cancer Cleanse online programs. He couldn’t believe his ears. I had to explain what each one of those things were.
Yes you can lose fat on a low carb because it’s just another low calorie diet. How do I know this? I’ve done low carb, (Atkins, etc) high carb, (Slimming Word) moderate carb etc and log my food and was shocked each time to see they were all low calorie. After the initial week or so the rate of fat loss is same as any other diet. It’s calories in calories out. Simple. It’s what some call indirect deficit diet placing silly restriction, rules can eat must eat etc. and of course you lose weight but nothing to do with low carb. It works because it’s a low calorie diet.
As in adults, glucose is the predominant cerebral fuel for the fetus and newborn. Studies in experimental animals and humans indicate that cerebral glucose utilization initially is low and increases with maturation with increasing regional heterogeneity. The increases in cerebral glucose utilization with advancing age occur as a consequence of increasing functional activity and cerebral energy demands… glucose plays a critical role in the developing brain, not only as the primary substrate for energy production but also to allow for normal biosynthetic processes to proceed.
The ketogenic diet has been studied in at least 14 rodent animal models of seizures. It is protective in many of these models and has a different protection profile than any known anticonvulsant. Conversely, fenofibrate, not used clinically as an antiepileptic, exhibits experimental anticonvulsant properties in adult rats comparable to the ketogenic diet. This, together with studies showing its efficacy in patients who have failed to achieve seizure control on half a dozen drugs, suggests a unique mechanism of action.