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.
As discussed in the first article of this series, ketosis is a metabolic state in which the brain switches to using ketone bodies – derived from the breakdown of fat – as its primary energy source, instead of glucose. This way body protein, which would otherwise be broken down and converted into glucose through the process of gluconeogenesis, are spared.
First, that study, which was reported upon widely, was on mice. Mice are not like humans in the way they fatten or contract metabolic diseases. Journalists/media should stop reporting on mice stories as if they were applicable to humans, especially when there is such a large body of clinical trial data on humans. Let’s be clear: rigorous clinical trial data on humans trumps any data on mice. Every time. And what does the rigorous data on humans say?