The original therapeutic diet for paediatric epilepsy provides just enough protein for body growth and repair, and sufficient calories[Note 1] to maintain the correct weight for age and height. The classic therapeutic ketogenic diet was developed for treatment of paediatric epilepsy in the 1920s and was widely used into the next decade, but its popularity waned with the introduction of effective anticonvulsant medications. This classic ketogenic diet contains a 4:1 ratio by weight of fat to combined protein and carbohydrate. This is achieved by excluding high-carbohydrate foods such as starchy fruits and vegetables, bread, pasta, grains, and sugar, while increasing the consumption of foods high in fat such as nuts, cream, and butter. Most dietary fat is made of molecules called long-chain triglycerides (LCTs). However, medium-chain triglycerides (MCTs)—made from fatty acids with shorter carbon chains than LCTs—are more ketogenic. A variant of the classic diet known as the MCT ketogenic diet uses a form of coconut oil, which is rich in MCTs, to provide around half the calories. As less overall fat is needed in this variant of the diet, a greater proportion of carbohydrate and protein can be consumed, allowing a greater variety of food choices.
Once “keto-adapted,” many tissues increase their capacity to utilize ketones for fuel. Some tissues even prefer to use ketones for their cellular energy needs. For instance, the heart, as well as many areas of the brain, prefers to use ketone bodies as opposed to glucose. One interesting fact is that Dr. Stephen Cunnane found that the uptake of ketone bodies in the brain is proportional to their production. Additional research has also demonstrated that as uptake of ketones increases, the uptake of glucose decreases in brain tissue. In contrast, there are certain cells that cannot use fatty acids or ketone bodies, and are considered “obligate glucose users.” Red blood cells and specific parts of the brain are obligate glucose users. Don’t stress, however, because even though you may not be consuming a lot of carbohydrates, these cells can obtain glucose through a biological process called gluconeogenesis (the production of glucose from other non-glucose materials).
Keto breath, on the other hand, is less of a side-effect and more of a harmless inconvenience (your breath literally smells like nail polish remover). Basically, when your body breaks down all that extra fat on the keto diet, it produces ketones—one of which is the chemical acetone, Keatley previously told WH. (Yes, the same stuff that's in nail polish remover.)
When you eat less than 50 grams of carbs a day, your body eventually runs out of fuel (blood sugar) it can use quickly. This typically takes 3 to 4 days. Then you’ll start to break down protein and fat for energy, which can make you lose weight. This is called ketosis. It's important to note that the ketogenic diet is a short term diet that's focussed on weight loss rather than the pursuit of health benefits.
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.
The confusion between ketosis and ketoacidosis is a prominent reason why many individuals, particularly doctors, steer clear of the keto diet for beginners. It’s important to understand that these are two very DIFFERENT metabolic states. Ketoacidosis may occur in uncontrolled type 1 diabetics (DKA; diabetic ketoacidosis) due to insulin deficiencies. DKA is associated with both elevated blood glucose and ketone levels; due to little to no insulin production, blood glucose cannot enter insulin-dependent cells to be used for energy, and as such, cells become hungry, resulting in uncontrolled ketone production. In turn, a highly acidic environment is created that can have detrimental effects on an individual’s health, possibly resulting in death. It must be echoed that the ketogenic diet, which induces “nutritional” ketosis, is vastly different and should never be confused with DKA. To put this in perspective, a normal state of ketosis, as achieved via the keto diet for beginners may elevate ketones anywhere from 0.3–5mM, while DKA results in ketone levels of about 15mM or higher.
Keto for Alzheimer’s Disease: One characteristic of Alzheimer’s disease is insulin resistance in the brain (hence why it’s now being referred to as type III diabetes), which robs this critical tissue of energy. Limiting glucose while introducing ketones may be an effective mechanism for replenishing the energy in the tissue. The higher level of ketone production accompanied with a ketogenic diet is another example as to why this diet is superior to one that simply restricts carbohydrate intake. Additionally, Alzheimer’s disease is characterized by beta-amyloid deposition, which may also be mitigated by the implementation of a ketogenic diet.
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. 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. For this group, and for children in particular, the diet has once again found a role in epilepsy management.
Increased Energy: Fat and ketone bodies can be utilized as a fuel source for nearly all of the cells in the body. Once the body begins to use ketones as its primary fuel source, there will be a noticeable increase in energy since you are avoiding the ups and downs associated with high-carbohydrate/high-glucose/high-insulin levels that result in feeling lethargic and tired throughout the day.
These affect your brain and spine, as well as the nerves that link them together. Epilepsy is one, but others may be helped by a ketogenic diet as well, including Alzheimer’s disease, Parkinson’s disease, and sleep disorders. Scientists aren’t sure why, but it may be that the ketones your body makes when it breaks down fat for energy help protect your brain cells from damage.
Many ketogenic dieters also swear by MCT oil. (MCT simply stands for medium chain triglycerides.) MCT's energy-sustaining powers can be explained as follows: When MCT oil is metabolized in the body, it behaves more like a carbohydrate than a fat. Unlike other fats, MCT oil does not go through the lymphatic system. Instead, it is transported directly to the liver where it is metabolized so it releases energy like a carbohydrate and creates lots of ketones (which can be used for fuel) in the process.
Wondering how u eat veggies without going over your carbs n how do you get all the fats in. I’ve put the requirements into my fitness pal(macros) but I’m still not losing. Mine are set at 5% carbs 25% protein n 70% fats. Don’t know what I’m doing wrong. I’m allergic to gluten some dairy n eggs. Any help would be great so I can start losing instead of gaining
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.