In addition to the seaweed and glycogen carbohydrates mentioned above, the Inuit can access many plant sources. The stomach contents of caribou contain a large quantity of partially digested lichens and plants, which the Inuit once considered a delicacy. They also harvested reindeer moss and other lichens directly. The extended daylight of the arctic summer led to a profusion of plant life, and they harvested plant parts including berries, roots and stems, as well as mushrooms. They preserved some gathered plant life to eat during winter, often by dipping it in seal fat.[71]
When HVMN Ketone was tested in mice, they performed 38% better on a maze solving challenge, so it's possible there may be a cognitive boost for humans also.9 While following a ketogenic diet, you avoid the energy peaks and troughs that come from quick-energy carbs. Producing ketones from stored body fat provides the brain with a steady, sustainable supply of fuel.
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).[19] 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.[56]
Here’s what we do know: The keto diet may be useful in treating symptoms of epilepsy, a seizure disorder. “The use of keto in treating epilepsy has the most evidence,” Angelone says. One study conducted by Johns Hopkins Medicine, for example, followed epileptic patients on the keto diet and found that 36 percent of them had a 50 percent reduction in seizures after three months on the diet, and 16 percent were seizure-free. However, experts aren't entirely sure why the keto diet has this affect, she adds.
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.[7]
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