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.
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.
As in adults, glucose is the predominant cerebral fuel for the fetus and newborn. Studies in experimental animals and humans indicate that cerebral glucose utilization initially is low and increases with maturation with increasing regional heterogeneity. The increases in cerebral glucose utilization with advancing age occur as a consequence of increasing functional activity and cerebral energy demands… glucose plays a critical role in the developing brain, not only as the primary substrate for energy production but also to allow for normal biosynthetic processes to proceed.
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.
People claiming huge benefits of these supplements – despite the lack of solid scientific support – may sometimes have a financial reason to believe in the supplements. Some of these products are sold under a multi-level marketing arrangement, where sales people are paid based on commission. For example, the company Prüvit sells drinkable ketones, called KETO//OS with a multi-level marketing structure.