Intermittent Fasting Neurology examines the specific effects of cyclical periods of food restriction on the structure, function, and resilience of the central nervous system. This field investigates how metabolic switching, primarily from glucose to ketone bodies, influences neuronal energy utilization, synaptic plasticity, and the expression of neuroprotective genes. Understanding this relationship is key to leveraging dietary timing as a non-pharmacological strategy for enhancing cognitive function and mitigating neurodegenerative risk. The neurological benefits are often mediated through shifts in systemic hormonal signaling, including insulin, IGF-1, and ghrelin.
Origin
This specialized term emerges from the intersection of nutritional science, endocrinology, and neuroscience, linking established fasting practices with modern molecular neurology. Early research focused primarily on the metabolic benefits of fasting, but recent attention has shifted to the profound, direct impact on brain cellular processes. It is a critical component of metabolic health strategies for brain longevity and cognitive reserve.
Mechanism
Fasting triggers a metabolic shift that increases the production of ketone bodies, such as beta-hydroxybutyrate, which serve as an efficient alternative fuel source for neurons. This metabolic state upregulates the expression of neurotrophic factors, particularly BDNF, which promotes the growth and survival of neurons and synapses. Furthermore, intermittent fasting enhances cellular autophagy, a vital process for clearing damaged organelles and proteins, thereby improving overall neuronal health and function.
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