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.
The nerve impulse is characterised by a great influx of sodium ions through channels in the neuron's cell membrane followed by an efflux of potassium ions through other channels. The neuron is unable to fire again for a short time (known as the refractory period), which is mediated by another potassium channel. The flow through these ion channels is governed by a "gate" which is opened by either a voltage change or a chemical messenger known as a ligand (such as a neurotransmitter). These channels are another target for anticonvulsant drugs.
Reduced hunger. Many people experience a marked reduction in hunger on a keto diet. This may be caused by an increased ability of the body to be fueled by its fat stores. Many people feel great when they eat just once or twice a day, and may automatically end up doing a form of intermittent fasting. This saves time and money, while also speeding up weight loss.
Early studies reported high success rates; in one study in 1925, 60% of patients became seizure-free, and another 35% of patients had a 50% reduction in seizure frequency. These studies generally examined a cohort of patients recently treated by the physician (a retrospective study) and selected patients who had successfully maintained the dietary restrictions. However, these studies are difficult to compare to modern trials. One reason is that these older trials suffered from selection bias, as they excluded patients who were unable to start or maintain the diet and thereby selected from patients who would generate better results. In an attempt to control for this bias, modern study design prefers a prospective cohort (the patients in the study are chosen before therapy begins) in which the results are presented for all patients regardless of whether they started or completed the treatment (known as intent-to-treat analysis).
First appointment: Your first meeting with our team will be a one-hour new patient appointment. You’ll meet our nurse practitioners, social worker and dietitians to discuss the diet’s daily requirements, the initiation process, the length of time your child will be on the diet, how the diet may affect your family and any other questions your family may have. If the ketogenic diet team and your family both agree the diet will be manageable for your family, an initiation is scheduled.
Note the emphasis on ketosis as a temporary adaptive state. Our ancestors could not be in fasting-induced ketosis permanently because they would eventually exhaust their fat reserves (which were presumably far more limited than ours, owing to the simple fact that they ate less and moved more than we do). They would then progress from fasting to starving, and subsequently die.
What about fruits and vegetables? All fruits are rich in carbs, but you can have certain fruits (usually berries) in small portions. Vegetables (also rich in carbs) are restricted to leafy greens (such as kale, Swiss chard, spinach), cauliflower, broccoli, Brussels sprouts, asparagus, bell peppers, onions, garlic, mushrooms, cucumber, celery, and summer squashes. A cup of chopped broccoli has about six carbs.
The Johns Hopkins Hospital protocol for initiating the ketogenic diet has been widely adopted. It involves a consultation with the patient and their caregivers and, later, a short hospital admission. Because of the risk of complications during ketogenic diet initiation, most centres begin the diet under close medical supervision in the hospital.
When you eat tons of carbs, your blood sugar is consistently elevated, and then so is insulin. Insulin is a hormone that keeps your blood sugar in check by shuttling the glucose into cells, but when there’s a consistently high amount of insulin, your cells become resistant. This insulin resistance makes it easier to store fat, and chronically high levels of insulin also cause excessive inflammation in the body, which contributes to heart disease, high blood pressure, and potentially type 2 diabetes.
While it’s true that low-carb diets do raise the so-called bad LDL-cholesterol in some people, it’s important to note that LDL-C, when influenced by diet, has never been shown to have any effect on cardiovascular risk. Large clinical trials and observational studies show that one’s level of LDL-C and the lowering of LDL-C through diet is not reliably linked to cardiovascular outcomes.21, 22, 23
Over 8–10 mmol/l: It’s normally impossible to get to this level just by eating a keto diet. It means that something is wrong. The most common cause by far is type 1 diabetes, with severe lack of insulin. Symptoms include feeling very sick with nausea, vomiting, abdominal pain and confusion. The possible end result, ketoacidosis, may be fatal and requires immediate medical care. Learn more