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.
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.”
The ketogenic diet is a high-fat, adequate-protein, low-carbohydrate diet that in medicine is used primarily to treat difficult-to-control (refractory) epilepsy in children. The diet forces the body to burn fats rather than carbohydrates. Normally, the carbohydrates contained in food are converted into glucose, which is then transported around the body and is particularly important in fueling brain function. However, if little carbohydrate remains in the diet, the liver converts fat into fatty acids and ketone bodies. The ketone bodies pass into the brain and replace glucose as an energy source. An elevated level of ketone bodies in the blood, a state known as ketosis, leads to a reduction in the frequency of epileptic seizures. Around half of children and young people with epilepsy who have tried some form of this diet saw the number of seizures drop by at least half, and the effect persists even after discontinuing the diet. Some evidence indicates that adults with epilepsy may benefit from the diet, and that a less strict regimen, such as a modified Atkins diet, is similarly effective. Potential side effects may include constipation, high cholesterol, growth slowing, acidosis, and kidney stones.
Full disclosure: I have followed a low-carb diet for nearly a decade and find no problem adhering to it. I’ve lost weight and all my cardiovascular biomarkers have improved. Moreover, I’ve studied the science and history behind low-carbohydrate diets, so beyond my personal experience, I bring an evidence-based perspective. (Previously, for 25+ years, I adhered faithfully to a “mostly plants” regimen of fruits, veggies, and whole grains, including my own homemade 7-grain bread, while exercising religiously. Yet during that time my blood lipids were unhealthy, and I never could shake an extra 10-20 pounds.)
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.
Normal dietary fat contains mostly long-chain triglycerides (LCTs). Medium-chain triglycerides (MCTs) are more ketogenic than LCTs because they generate more ketones per unit of energy when metabolised. Their use allows for a diet with a lower proportion of fat and a greater proportion of protein and carbohydrate, leading to more food choices and larger portion sizes. The original MCT diet developed by Peter Huttenlocher in the 1970s derived 60% of its calories from MCT oil. Consuming that quantity of MCT oil caused abdominal cramps, diarrhea, and vomiting in some children. A figure of 45% is regarded as a balance between achieving good ketosis and minimising gastrointestinal complaints. The classical and modified MCT ketogenic diets are equally effective and differences in tolerability are not statistically significant. The MCT diet is less popular in the United States; MCT oil is more expensive than other dietary fats and is not covered by insurance companies.
The classic ketogenic diet is not a balanced diet and only contains tiny portions of fresh fruit and vegetables, fortified cereals, and calcium-rich foods. In particular, the B vitamins, calcium, and vitamin D must be artificially supplemented. This is achieved by taking two sugar-free supplements designed for the patient's age: a multivitamin with minerals and calcium with vitamin D. A typical day of food for a child on a 4:1 ratio, 1,500 kcal (6,300 kJ) ketogenic diet comprises three small meals and three small snacks:
Sleep enough – for most people at least seven hours per night on average – and keep stress under control. Sleep deprivation and stress hormones raise blood sugar levels, slowing ketosis and weight loss a bit. Plus they might make it harder to stick to a keto diet, and resist temptations. So while handling sleep and stress will not get you into ketosis on it’s own, it’s still worth thinking about.