Supplemental ketosis: This form of ketosis has recently gained momentum in the field of ketogenic dieting. Supplemental ketosis is a ketogenic state that is achieved through the ingestion of ketogenic supplements. Consuming these substances alone does not mean that an individual is “keto-adapted.” While these products can help during the keto-adaptation period, especially if one is experiencing the “keto-flu,” they will only elicit short-term increases in blood ketone levels. Exogenous ketones can acutely produce benefits similar to the ketogenic diet; however, these products are best used in conjunction with a well-formulated keto diet for beginners, or the very at least, a diet that restricts carbohydrates. The commonly used supplements on the market are medium-chain triglyceride (MCT) oil and exogenous ketones. MCT oil is a fat that, in contrast to other longer-chain fatty acids, travels straight from the intestines to the liver where it is readily metabolized. This allows for ketone production in the liver to occur faster than with other fats (long-chain fatty acids have to travel through the lymph and circulatory systems first). Exogenous ketones are synthetic substances that mimic the ketones produced in our body (endogenous ketones). Exogenous ketones can come in the form of ketone salts or ketone esters.
By cutting carb intake significantly, we can drastically reduce insulin resistance, the precursor to type 2 diabetes. In addition, low carb diets, along with exercise, can be very effective at helping alleviate the symptoms and progression of type 2 diabetes. Beyond that, ketosis itself is appetite-suppressing, meaning your hunger will naturally check itself, increasing your caloric deficit and making you lose fat even faster. Read more about ketosis: What Is Ketosis, and How Long Does It Take to Get into Ketosis?
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.