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Let’s meditate for a second. Close your eyes. What do you see when you picture yourself on keto? Naturally, carb deprivation has carved out Michelangelo's David from your block of pudgy carrara marble. You have so much more energy now, thanks to the chunk of grass-fed butter (or ghee!) you’ve slid into your morning coffee. You're so spry, in fact, that you’re considering investing in bitcoin even though you’re late to the game, or writing a novel even though you don’t read, or getting into a relationship just because you’re overwhelmed by the trove of eligible suitors now bashfully small-smiling at you on public transport.

A study with an intent-to-treat prospective design was published in 1998 by a team from the Johns Hopkins Hospital[20] and followed-up by a report published in 2001.[21] As with most studies of the ketogenic diet, no control group (patients who did not receive the treatment) was used. The study enrolled 150 children. After three months, 83% of them were still on the diet, 26% had experienced a good reduction in seizures, 31% had had an excellent reduction, and 3% were seizure-free.[Note 7] At 12 months, 55% were still on the diet, 23% had a good response, 20% had an excellent response, and 7% were seizure-free. Those who had discontinued the diet by this stage did so because it was ineffective, too restrictive, or due to illness, and most of those who remained were benefiting from it. The percentage of those still on the diet at two, three, and four years was 39%, 20%, and 12%, respectively. During this period, the most common reason for discontinuing the diet was because the children had become seizure-free or significantly better. At four years, 16% of the original 150 children had a good reduction in seizure frequency, 14% had an excellent reduction, and 13% were seizure-free, though these figures include many who were no longer on the diet. Those remaining on the diet after this duration were typically not seizure-free, but had had an excellent response.[21][22]
The ketogenic diet reduces seizure frequency by more than 50% in half of the patients who try it and by more than 90% in a third of patients.[18] Three-quarters of children who respond do so within two weeks, though experts recommend a trial of at least three months before assuming it has been ineffective.[9] Children with refractory epilepsy are more likely to benefit from the ketogenic diet than from trying another anticonvulsant drug.[1] Some evidence indicates that adolescents and adults may also benefit from the diet.[9]

Let’s meditate for a second. Close your eyes. What do you see when you picture yourself on keto? Naturally, carb deprivation has carved out Michelangelo's David from your block of pudgy carrara marble. You have so much more energy now, thanks to the chunk of grass-fed butter (or ghee!) you’ve slid into your morning coffee. You're so spry, in fact, that you’re considering investing in bitcoin even though you’re late to the game, or writing a novel even though you don’t read, or getting into a relationship just because you’re overwhelmed by the trove of eligible suitors now bashfully small-smiling at you on public transport.


And it all culminated with me stepping into Dr. Jeff Volek’s world famous laboratory at University of Connecitut to subject myself to extensive blood testing, chunks of muscle removed from my legs, fat sucked out of my butt-cheeks, urine, stool and gut microbiome testing, oxygen and carbon dioxide testing and countless hours of treadmill running to discover what a full twelve months of eating a ketotic diet had actually done to my body.
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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