We have known for decades the positive effects of ketogenic diets upon epilepsy and other seizure disorders. Slowly we are beginning to correlate inflammatory conditions and immune dysfunction with ASD and other neurological disease risks in children.
So how does this work?
Ketogenic diets in essence restrict glycolysis and increases fatty acid oxidation forcing the neurological cells to rely upon the resulting ketone bodies for energy vs. glucose.
These ketone bodies seem to enhance cellular metabolism and improve mitochondrial function. This alternative energy pathway contributes to a cascade effect of much needed processes lacking in those with neuroinflammatory and mitochondrial diseases such as autism spectrum disorder, Alzheimer's disease, Parkinson's disease, epilepsy and ALS.
It is thought that Ketone bodies via increased cellular signaling assist with restoration of neurotransmitter and ion channel functions. Ketone bodies also change metabolism and neuronal excitability thought to increase ATP. Increasing ATP ultimately raises adenosine levels in the brain and restores DNA methylation. Ketone bodies also influence regulatory effects upon glutamate by blunting it's release.
Research shows that adenosine plays a major role in cognition often a symptom of neurological conditions and glutamate in high doses can contribute to agitation, social anxieties, insomnia, severe mood swings, mania and addictive behaviors.
The ketone bodies generated from the diet seem to alter the brains processing of glutamate, an excitatory neurotransmitter. Through a complex process it seems as if ketones trigger more production of GABA which assists with a glutamate purge. The benefit is less provocation by an excitatory neurotransmitter.
Adenosine can translate ketone provoked metabolic changes into enhanced energy metabolism of the brain.
Anecdotally as a practice, we find positive changes with cognition and sociability with our autism spectrum disorder population and less inflammatory symptoms in our chronic tick-borne illnesses and autoimmune disease patients.
