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, 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. 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. 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.
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.
High levels of circulating ketones may have a direct appetite-suppressant effect. In fact, the exogenous ketone ester used in HVMN Ketone rapidly increased blood levels of beta-hydroxybutyrate and lowered appetite as well as levels of ghrelin - the hormone that increases hunger. While this still needs to be explored further, it is possible that exogenous ketones may be useful for appetite control as part of a holistic weight loss strategy.11
Some people group tomatoes with vegetables, but a tomato is actually a fruit. Low in fat but also carbs (with just 2.4 g of net carbs per ½ cup), tomatoes are also keto-friendly. The same serving size of tomatoes contains 2.4 g of sugar and 16 calories. Among their health benefits, tomatoes contain lycopene, which research suggests may help prevent heart disease.
Decades later, when low carb became the best thing since sliced bread, people were calling it the Air Force Diet and the Drinking Man’s; Atkins and Paleo; Comet and Cupid. Then, in 2016, podcaster and MMA commentator Joe Rogan discussed keto once on his show and his loyal following of fitness enthusiasts and life optimizers took it and ran (especially in the mornings, to increase fat burning during the fasting state).
And it’s not an easy diet to stick to, even in the short term. Fell pointed me to a series of articles he’d written after talking to scientists about low-carb diets. As a former track runner myself, I wasn’t surprised to hear him say that carb depletion is terrible for athletes, nor did it come as a shock to hear that fat isn’t necessarily going to make you feel “fuller for longer.”
Protein will induce an insulin response in the body, if consumed in high amounts. The most intuitive way to start a keto diet for most people is by removing all of the carbs they have been eating. Typically people will replace those calories by increasing their lean meat consumption. That's a recipe for disaster! Keeping protein moderate is an often overlooked, but very important part of a keto diet. Most people need around 0.6g to 1.0g of protein per pound of lean body mass.
And what I’m writing has nothing to do with taking supplements to induce ketosis or whatever. I believe these things are covered in Volek & Phoney’s book The Art and Science of Low Carb Living, which I would have thought you to be very familiar with. The iodine stuff you can read about in Iodine, Why We Need, Why We Can’t Live Without It by Brownstein.
Fascinating stuff and I am quite curious how we know for certain one is actually in ketosis i.e. using ketones as primary fuel source BECAUSE we do know that glucose has a shorter metabolic pathway to burn and under most conditions, given the presence of glucose, that is what the body will default to which is why high fat and high sugar together in diet is so detrimental. So if we use one or more of the above “boosters” and show high levels of blood ketones but also highish levels of glucose (during initial transition) will be mostly burning ketones or still defaulting to glucose?
1. If a set number ketones in the blood is an indicator that my body has transitioned to ketosis and not necessarily the cause (the cause being limited access to glycogen because of limited carb intake) then how does using exogenous ketones put me in ketosis as opposed to mimic being in ketosis (because when measuring blood ketones suddenly there are more because I put them there, I didn’t create them)?