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There are many ways in which epilepsy occurs. Examples of pathological physiology include: unusual excitatory connections within the neuronal network of the brain; abnormal neuron structure leading to altered current flow; decreased inhibitory neurotransmitter synthesis; ineffective receptors for inhibitory neurotransmitters; insufficient breakdown of excitatory neurotransmitters leading to excess; immature synapse development; and impaired function of ionic channels.
#5) It can level up your brain, including positively counteracting conditions like Parkinson’s, Alzheimer’s, and dementia. As explained here in this TEDx talk by Mark Mattson, Professor at Johns Hopkins University and Chief of the Laboratory of Neurosciences at the National Institute on Aging, fasting is grounded in serious research and more studies are coming out showing the benefits:
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.
The ketogenic diet is usually initiated in combination with the patient's existing anticonvulsant regimen, though patients may be weaned off anticonvulsants if the diet is successful. Some evidence of synergistic benefits is seen when the diet is combined with the vagus nerve stimulator or with the drug zonisamide, and that the diet may be less successful in children receiving phenobarbital.
Wilder's colleague, paediatrician Mynie Gustav Peterman, later formulated the classic diet, with a ratio of one gram of protein per kilogram of body weight in children, 10–15 g of carbohydrate per day, and the remainder of calories from fat. Peterman's work in the 1920s established the techniques for induction and maintenance of the diet. Peterman documented positive effects (improved alertness, behaviour, and sleep) and adverse effects (nausea and vomiting due to excess ketosis). The diet proved to be very successful in children: Peterman reported in 1925 that 95% of 37 young patients had improved seizure control on the diet and 60% became seizure-free. By 1930, the diet had also been studied in 100 teenagers and adults. Clifford Joseph Barborka, Sr., also from the Mayo Clinic, reported that 56% of those older patients improved on the diet and 12% became seizure-free. Although the adult results are similar to modern studies of children, they did not compare as well to contemporary studies. Barborka concluded that adults were least likely to benefit from the diet, and the use of the ketogenic diet in adults was not studied again until 1999.
I would like to know what led you to the conclusion to recommend eating in the morning and fasting in the evening instead of the other way around. You do not link any studies here that show TRF in the morning is better than TRF in the evening. You do state “Nighttime eating is well associated with a higher risk of obesity, as well as diabetes.” but I would hazard a guess that alot people that snack into the evening have many other factors at play that could effect their risk of obesity and diabetes and are possibly not fasting at all. I have been doing TRF from 12-8pm every day for almost a year and have seen vast improvements in my health, not least of which is a loss of 70 lbs, so it seems odd to read items 3 and 4 on your 4 ways to use this information for better health. If you have evidence that supports the idea that TRF in the evening is bad then I would like to see it and perhaps change my dieting habbits.