On the ketogenic diet, carbohydrates are restricted and so cannot provide for all the metabolic needs of the body. Instead, fatty acids are used as the major source of fuel. These are used through fatty-acid oxidation in the cell's mitochondria (the energy-producing parts of the cell). Humans can convert some amino acids into glucose by a process called gluconeogenesis, but cannot do this by using fatty acids. Since amino acids are needed to make proteins, which are essential for growth and repair of body tissues, these cannot be used only to produce glucose. This could pose a problem for the brain, since it is normally fuelled solely by glucose, and most fatty acids do not cross the blood–brain barrier. However, the liver can use long-chain fatty acids to synthesise the three ketone bodies β-hydroxybutyrate, acetoacetate and acetone. These ketone bodies enter the brain and partially substitute for blood glucose as a source of energy.
When you eat foods high in carbohydrates and fat, your body naturally produces glucose. Carbohydrates are the easiest thing for the body to process, and therefore it will use them first – resulting in the excess fats to be stored immediately. In turn, this causes weight gain and health problems that are associated with high fat, high carbohydrate diets (NOT keto).
First reported in 2003, the idea of using a form of the Atkins diet to treat epilepsy came about after parents and patients discovered that the induction phase of the Atkins diet controlled seizures. The ketogenic diet team at Johns Hopkins Hospital modified the Atkins diet by removing the aim of achieving weight loss, extending the induction phase indefinitely, and specifically encouraging fat consumption. Compared with the ketogenic diet, the modified Atkins diet (MAD) places no limit on calories or protein, and the lower overall ketogenic ratio (about 1:1) does not need to be consistently maintained by all meals of the day. The MAD does not begin with a fast or with a stay in hospital and requires less dietitian support than the ketogenic diet. Carbohydrates are initially limited to 10 g per day in children or 20 g per day in adults, and are increased to 20–30 g per day after a month or so, depending on the effect on seizure control or tolerance of the restrictions. Like the ketogenic diet, the MAD requires vitamin and mineral supplements and children are carefully and periodically monitored at outpatient clinics.
A striking new study published in the journal Diabetes suggests that simply blasting the air conditioner or turning down the heat in winter may help us attack belly fat while we sleep. Colder temperatures subtly enhance the effectiveness of our stores of brown fat—fat keeps you warm by helping you burn the fat stored in your belly. Participants spent a few weeks sleeping in bedrooms with varying temperatures: a neutral 75 degrees, a cool 66 degrees, and a balmy 81 degrees. After four weeks of sleeping at 66 degrees, the subjects had almost doubled their volumes of brown fat. (And yes, that means they lost belly fat.) And speaking of turbocharging your body’s fat burn, learn how stubborn weight gain may not be your fault, and turn off your hunger hormones with these powerful 20 Foods That Shut Off Your Hunger Hormones Fast!
There are so many tricks, shortcuts, and gimmicks out there on achieving optimal ketosis – I’d suggest you don’t bother with any of that. Optimal ketosis can be accomplished through dietary nutrition alone (aka just eating food). You shouldn’t need a magic pill to do it. Just stay strict, remain vigilant, and be focused on recording what you eat (to make sure your carb and protein intake are correct).
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).