Therapeutic ketosis and the broad field of applications for | 50758
International Research Journals

Therapeutic ketosis and the broad field of applications for theketogenic diet: Ketone ester applications & clinical updates


Raffaele Pilla

It has been recently shown that nutritional ketosis is effective against seizure disorders and various acute/chronic neurological disorders.
Physiologically, glucose is the primary metabolic fuel for cells. However, many neurodegenerative disorders have been associated with
impaired glucose transport/metabolism and with mitochondrial dysfunction, such as Alzheimer’s/Parkinson’s disease, general seizure
disorders, and traumatic brain injury. Ketone bodies and tricarboxylic acid cycle intermediates represent alternative fuels for the brain and
can bypass the rate-limiting steps associated with impaired neuronal glucose metabolism. Therefore, therapeutic ketosis can be considered
as a metabolic therapy by providing alternative energy substrates. It has been estimated that the brain derives over 60% of its total energy
from ketones when glucose availability is limited. In fact, after prolonged periods of fasting or ketogenic diet (KD), the body utilizes energy
obtained from free fatty acids (FFAs) released from adipose tissue. Because the brain is unable to derive significant energy from FFAs, hepatic
ketogenesis converts FFAs into ketone bodies-hydroxybutyrate (BHB) and acetoacetate (AcAc)-while a percentage of AcAc spontaneously
decarboxylates to acetone. Large quantities of ketone bodies accumulate in the blood through this mechanism. This represents a state of
normal physiological ketosis and can be therapeutic. Ketone bodies are transported across the blood-brain barrier by monocarboxylic acid
transporters to fuel brain function. Starvation or nutritional ketosis is an essential survival mechanism that ensures metabolic flexibility during
prolonged fasting or lack of carbohydrate ingestion. Therapeutic ketosis leads to metabolic adaptations that may improve brain metabolism,
restore mitochondrial ATP production, decrease reactive oxygen species production, reduce inflammation, and increase neurotrophic
factors’ function. It has been shown that KD mimics the effects of fasting and the lack of glucose/insulin signaling, promoting a metabolic
shift towards fatty acid utilization. In this work, the author reports a number of successful case reports treated through metabolic ketosis.

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