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3rd International Conference on
Health Care and
Health Management
Joint Event
&
November 04-05, 2019 | Prague, Czech Republic
6th International Conference on
Neuroscience and
Neurological Disorders
Journal of Neurology and Clinical Neuroscience | Volume 3
Therapeutic ketosis and the broad field of applications for the ketogenic diet:
Ketone ester applications & clinical updates
Raffaele Pilla
St. John of God Hospital, Italy
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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