The first modern study of fasting as a treatment for epilepsy was in France in 1911.[12] Twenty epilepsy patients of all ages were "detoxified" by consuming a low-calorie vegetarian diet, combined with periods of fasting and purging. Two benefited enormously, but most failed to maintain compliance with the imposed restrictions. The diet improved the patients' mental capabilities, in contrast to their medication, potassium bromide, which dulled the mind.[13]
In nutrition, diet is the sum of food consumed by a person or other organism.[1] The word diet often implies the use of specific intake of nutrition for health or weight-management reasons (with the two often being related). Although humans are omnivores, each culture and each person holds some food preferences or some food taboos. This may be due to personal tastes or ethical reasons. Individual dietary choices may be more or less healthy.
During the 1920s and 1930s, when the only anticonvulsant drugs were the sedative bromides (discovered 1857) and phenobarbital (1912), the ketogenic diet was widely used and studied. This changed in 1938 when H. Houston Merritt, Jr. and Tracy Putnam discovered phenytoin (Dilantin), and the focus of research shifted to discovering new drugs. With the introduction of sodium valproate in the 1970s, drugs were available to neurologists that were effective across a broad range of epileptic syndromes and seizure types. The use of the ketogenic diet, by this time restricted to difficult cases such as Lennox–Gastaut syndrome, declined further.[10]
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]
Some cultures and religions have restrictions concerning what foods are acceptable in their diet. For example, only Kosher foods are permitted by Judaism, and Halal foods by Islam. Although Buddhists are generally vegetarians, the practice varies and meat-eating may be permitted depending on the sects.[2] In Hinduism, vegetarianism is the ideal. Jains are strictly vegetarian and consumption of roots is not permitted.
Children who discontinue the diet after achieving seizure freedom have about a 20% risk of seizures returning. The length of time until recurrence is highly variable, but averages two years. This risk of recurrence compares with 10% for resective surgery (where part of the brain is removed) and 30–50% for anticonvulsant therapy. Of those who have a recurrence, just over half can regain freedom from seizures either with anticonvulsants or by returning to the ketogenic diet. Recurrence is more likely if, despite seizure freedom, an electroencephalogram shows epileptiform spikes, which indicate epileptic activity in the brain but are below the level that will cause a seizure. Recurrence is also likely if an MRI scan shows focal abnormalities (for example, as in children with tuberous sclerosis). Such children may remain on the diet longer than average, and children with tuberous sclerosis who achieve seizure freedom could remain on the ketogenic diet indefinitely.[46]
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.[7]
Grazing between meals used to be on the weight-loss hit list. But nutritionists now know that it's better to satisfy a craving with healthy grub than ignore it and risk a junk-food binge later. The best picks are filling, protein-packed snacks, such as one stick of string cheese, a tablespoon of peanut butter on a piece of fruit, or a medium-size bowl of edamame.
Also, the natural sugar in fruit does affect your carbohydrate intake — especially if you eat a lot of fruit. This may temporarily raise your blood sugar or certain blood fats. However, this effect is lessened if you are losing weight. If you have diabetes or any other health conditions or concerns, work with your doctor to adjust the Mayo Clinic Diet for your situation. For example, people with diabetes should aim for more vegetables than fruits, if possible. It's a good idea to snack on vegetables, rather than snacking only on fruit.
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.[7]
The word diet first appeared in English in the 13th century. Its original meaning was the same as in modern English, “habitually taken food and drink.” But diet was used in another sense too in the Middle and early modern English periods to mean “way of living.” This is, in fact, the original meaning of diet’s Greek ancestor diaita, which is derived from the verb diaitasthan, meaning “to lead one’s life.” In Greek, diaita, had already come to be used more specifically for a way of living prescribed by a physician, a diet, or other regimen.
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