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.
Long-term use of the ketogenic diet in children increases the risk of slowed or stunted growth, bone fractures, and kidney stones. The diet reduces levels of insulin-like growth factor 1, which is important for childhood growth. Like many anticonvulsant drugs, the ketogenic diet has an adverse effect on bone health. Many factors may be involved such as acidosis and suppressed growth hormone. About one in 20 children on the ketogenic diet develop kidney stones (compared with one in several thousand for the general population). A class of anticonvulsants known as carbonic anhydrase inhibitors (topiramate, zonisamide) are known to increase the risk of kidney stones, but the combination of these anticonvulsants and the ketogenic diet does not appear to elevate the risk above that of the diet alone. The stones are treatable and do not justify discontinuation of the diet. Johns Hopkins Hospital now gives oral potassium citrate supplements to all ketogenic diet patients, resulting in one-seventh of the incidence of kidney stones. However, this empiric usage has not been tested in a prospective controlled trial. Kidney stone formation (nephrolithiasis) is associated with the diet for four reasons:
Insulin is a hormone that lets your body use or store sugar as fuel. Ketogenic diets make you burn through this fuel quickly, so you don’t need to store it. This means your body needs -- and makes -- less insulin. Those lower levels may help protect you against some kinds of cancer or even slow the growth of cancer cells. More research is needed on this, though.
A slew of articles in recent months have referred to the ketogenic diet as a “fad” or “trend.” It’s “dangerous,” claimed one article, and an anonymous post by the Harvard Public School of Public Health said the diet “comes with serious risks.”1 Yet strangely, these critics seldom cite scientists or doctors who work with the diet, and many—including the Harvard article—cite no medical literature to substantiate their allegations. Without substantiation, many simply rehash long-contradicted, outdated claims.
Meanwhile, more than 70 trials have examined the health effects of a low-carb diet. They attest to the benefits64 associated with ketosis and low-carb diets, including a reduction in body weight and body mass index, improved cardiovascular risk factors including blood pressure, and the reversal of Type 2 diabetes. It is virtually impossible to imagine that a diet with so many health improvements in the ‘near term’ (2 years) could ultimately shorten life—and the study authors offer no possible mechanism to explain how this might happen.
In the 1960s, medium-chain triglycerides (MCTs) were found to produce more ketone bodies per unit of energy than normal dietary fats (which are mostly long-chain triglycerides). MCTs are more efficiently absorbed and are rapidly transported to the liver via the hepatic portal system rather than the lymphatic system. The severe carbohydrate restrictions of the classic ketogenic diet made it difficult for parents to produce palatable meals that their children would tolerate. In 1971, Peter Huttenlocher devised a ketogenic diet where about 60% of the calories came from the MCT oil, and this allowed more protein and up to three times as much carbohydrate as the classic ketogenic diet. The oil was mixed with at least twice its volume of skimmed milk, chilled, and sipped during the meal or incorporated into food. He tested it on 12 children and adolescents with intractable seizures. Most children improved in both seizure control and alertness, results that were similar to the classic ketogenic diet. Gastrointestinal upset was a problem, which led one patient to abandon the diet, but meals were easier to prepare and better accepted by the children. The MCT diet replaced the classic ketogenic diet in many hospitals, though some devised diets that were a combination of the two.
I’m discouraged to see that nowhere in the article nor in the comments is there a mention of a diet’s best fit to genetics. Consider if someone is an APOE E2 carrier and/or has certain polymorphisms of the APO5 gene. These are quite rare in Okinawa but much more prevalent in the USA (12% of the population). According to a number of well-designed studies, these genetic characteristics point to a higher fat, lower carbohydrate diet as beneficial and even a “moderate” carb diet as problematic.
If you’re wondering about the difference between ketosis and diabetic ketoacidosis, you’re not alone. “The word ketone is scary for most people with type 1 diabetes because they relate ketones to diabetic ketoacidosis,” says Patti Urbanski, MEd, RD, CDE, a certified diabetes educator with St. Luke’s Hospital in Duluth, Minnesota. “But with the ketogenic diet, we’re talking about a much lower level of ketones.”
Although many hypotheses have been put forward to explain how the ketogenic diet works, it remains a mystery. Disproven hypotheses include systemic acidosis (high levels of acid in the blood), electrolyte changes and hypoglycaemia (low blood glucose). Although many biochemical changes are known to occur in the brain of a patient on the ketogenic diet, it is not known which of these has an anticonvulsant effect. The lack of understanding in this area is similar to the situation with many anticonvulsant drugs.
Here’s the real kicker: the reason why the Inuit don’t go into ketosis as readily as other ethnic groups is the high prevalence of a deleterious mutation in the CPT1A gene. This mutation permitted adaptation to a high fat, low carbohydrate diet in the sense that those carrying the gene could survive to reproductive age while eating a diet entirely at odds with our evolutionary history. However this gene is associated with high infant mortality rates due to hypoketotic hypoglycemia: when Inuit babies’ blood glucose levels drop, they are unable to utilize ketone bodies to sustain their brains. The very mutation that permits adult survival in extreme circumstances compromises infant health – a powerful example of the trade-offs inherent to evolution. Humans can indeed adapt to an extreme environment and an extreme diet, but that adaptation comes at a high cost.
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.
One downside to a ketogenic diet for weight loss is the difficulty maintaining it. “Studies show that weight loss results from being on a low-carb diet for more than 12 months tend to be the same as being on a normal, healthy diet,” says Mattinson. While you may be eating more satiating fats (like peanut butter, regular butter, or avocado), you’re also way more limited in what’s allowed on the diet, which can make everyday situations, like eating dinner with family or going out with friends, far more difficult. Because people often find it tough to sustain, it’s easy to rely on it as a short-term diet rather than a long-term lifestyle.