Electrolytes: To reiterate, maintaining electrolyte balances is critical on a ketogenic diet, in order to prevent side effects and the “keto-flu.” While this can be done exclusively through whole foods, some individuals may require additional sources. Sodium, magnesium, potassium, and in some cases, calcium, can all be replenished via supplementation.
The confusion between ketosis and ketoacidosis is a prominent reason why many individuals, particularly doctors, steer clear of the keto diet for beginners. It’s important to understand that these are two very DIFFERENT metabolic states. Ketoacidosis may occur in uncontrolled type 1 diabetics (DKA; diabetic ketoacidosis) due to insulin deficiencies. DKA is associated with both elevated blood glucose and ketone levels; due to little to no insulin production, blood glucose cannot enter insulin-dependent cells to be used for energy, and as such, cells become hungry, resulting in uncontrolled ketone production. In turn, a highly acidic environment is created that can have detrimental effects on an individual’s health, possibly resulting in death. It must be echoed that the ketogenic diet, which induces “nutritional” ketosis, is vastly different and should never be confused with DKA. To put this in perspective, a normal state of ketosis, as achieved via the keto diet for beginners may elevate ketones anywhere from 0.3–5mM, while DKA results in ketone levels of about 15mM or higher.
As with other customized properties of the diet, the consumption of dairy is individualized. If digestive or glycemic problems develop due to the lactose and casein in dairy, then dairy may need to be avoided. If you can tolerate it, opt for lower carbohydrate dairy like cheese, heavy whipping cream, and butter, rather than higher carbohydrate products like milk.
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.[7]
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