This is the specialized area of research investigating the direct and indirect effects of a high-fat, very low-carbohydrate diet on brain function, metabolism, and neurological disorders. The primary mechanism involves shifting the brain’s fuel source from glucose to ketone bodies, such as beta-hydroxybutyrate (BHB). Clinically, this approach is studied for its potential to enhance cognitive performance and provide neuroprotection in conditions like epilepsy and Alzheimer’s disease.
Origin
The ketogenic diet originated in the 1920s as a medical intervention for refractory epilepsy, based on the observation that fasting could reduce seizure frequency. The ‘neuroscience’ component is a modern addition, focusing on the molecular and cellular mechanisms of ketone bodies within the central nervous system. This area represents the intersection of nutritional science and clinical neurology.
Mechanism
Ketone bodies, particularly BHB, serve as a highly efficient alternative fuel source for neurons, potentially bypassing impaired glucose metabolism pathways. BHB also acts as a signaling molecule, inhibiting histone deacetylases (HDACs) to promote the expression of neuroprotective genes, including BDNF. Furthermore, the metabolic state induced by the diet is associated with reduced oxidative stress and decreased neuroinflammation, contributing to neuronal stability.
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