Physicians of ancient Greece treated diseases, including epilepsy, by altering their patients' diet. An early treatise in the Hippocratic Corpus, On the Sacred Disease, covers the disease; it dates from c. 400 BC. Its author argued against the prevailing view that epilepsy was supernatural in origin and cure, and proposed that dietary therapy had a rational and physical basis.[Note 3] In the same collection, the author of Epidemics describes the case of a man whose epilepsy is cured as quickly as it had appeared, through complete abstinence of food and drink.[Note 4] The royal physician Erasistratus declared, "One inclining to epilepsy should be made to fast without mercy and be put on short rations."[Note 5] Galen believed an "attenuating diet"[Note 6] might afford a cure in mild cases and be helpful in others.
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I’m discouraged to see that nowhere in the article nor in the comments is there a mention of a diet’s best fit to genetics. Consider if someone is an APOE E2 carrier and/or has certain polymorphisms of the APO5 gene. These are quite rare in Okinawa but much more prevalent in the USA (12% of the population). According to a number of well-designed studies, these genetic characteristics point to a higher fat, lower carbohydrate diet as beneficial and even a “moderate” carb diet as problematic.
Implementing the diet can present difficulties for caregivers and the patient due to the time commitment involved in measuring and planning meals. Since any unplanned eating can potentially break the nutritional balance required, some people find the discipline needed to maintain the diet challenging and unpleasant. Some people terminate the diet or switch to a less demanding diet, like the modified Atkins diet or the low-glycaemic index treatment diet, because they find the difficulties too great.
No human population has ever lived in a permanent state of ketosis. Ketogenic diets are dangerous for pregnant women and developing fetuses, and the only human population that has ever subsisted on this dietary pattern advocated by keto diet proponents could only do so because of a genetic mutation that prevents them from going into ketosis. Unfortunately, it has the unintended but unavoidable consequence of reducing the survival prospects of their infants.
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.
"The keto diet is primarily used to help reduce the frequency of epileptic seizures in children. While it also has been tried for weight loss, only short-term results have been studied, and the results have been mixed. We don't know if it works in the long term, nor whether it's safe," warns registered dietitian Kathy McManus, director of the Department of Nutrition at Harvard-affiliated Brigham and Women's Hospital.
No animal on earth lives permanently in ketosis. Omnivorous animals such as bears and dogs, and obligate carnivores such as cats – the ultimate low-carbers – use gluconeogenesis to transform amino acids from protein into glucose. This allows them to maintain optimal blood glucose levels to fulfill their bodies’ needs for this vital nutrient. Only in prolonged starvation or a diabetic state will these animals enter ketosis.
As discussed in the first article of this series, ketosis is a metabolic state in which the brain switches to using ketone bodies – derived from the breakdown of fat – as its primary energy source, instead of glucose. This way body protein, which would otherwise be broken down and converted into glucose through the process of gluconeogenesis, are spared.
There is nothing inherently difficult about following a ketogenic diet. We have many patients who do this very easily over many years. The metabolic benefits significantly outway any perceived challenges from limiting particular food types. Uptake would be far more widespread if nutrition professionals left their predujical opinions of SFA’s behind. Finally, given the expertise in Ketogenic Diets at Harvard, Dr David Ludwig, for one springs to mind, I am surprised the author did not avail themselves of the local expertise.
First, that study, which was reported upon widely, was on mice. Mice are not like humans in the way they fatten or contract metabolic diseases. Journalists/media should stop reporting on mice stories as if they were applicable to humans, especially when there is such a large body of clinical trial data on humans. Let’s be clear: rigorous clinical trial data on humans trumps any data on mice. Every time. And what does the rigorous data on humans say?
Some sugar-free candy may seem safe (especially on dirty keto), but can contain the wrong sugar alcohols that could spike your blood glucose. This recipe uses stevia, which ranks much lower on the glycemic index, combined with lemon juice and gelatin for a chewy 3-ingredient gummy candy that still satisfies your sugar cravings. Make sure your gelatin comes from a pastured source to keep this one Bulletproof.
In terms of weight loss, you may be interested in trying the ketogenic diet because you’ve heard that it can make a big impact right away. And that’s true. “Ketogenic diets will cause you to lose weight within the first week,” says Mattinson. She explains that your body will first use up all of its glycogen stores (the storage form of carbohydrate). With depleted glycogen, you’ll drop water weight. While it can be motivating to see the number on the scale go down (often dramatically), do keep in mind that most of this is water loss initially.