- Jan 31, 2019
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Thanks for the info!Improved cognitive function is one of the most studied aspects of ketosis. The brain actually prefers to function on ketones. They are more efficient and produce less "emission" then glycogen. That's why it is so effective for epileptics.
Here's just a quick quote from a ncbi paper. I'm sure there's better. If you actually wanted to do a deep dive on the subject you will find an insane amount of info supporting the position that cognitive function improves on ketones.
While the PFC and HPC show distinct mechanisms of age-related dysfunction, one variable that appears to be ubiquitous across regions is a declining ability to utilize glucose as an energy substrate. Notably, glucose metabolism within the brain is significantly lower in aged study participants (Petit-Taboué et al., 1998; Gold, 2005; Rasgon et al., 2005) and this decline correlates with impaired behavior on the HPC-dependent Morris watermaze task and a spatial alternation task (Gage et al., 1984; Gold, 2005). Furthermore, cognitively impaired aged rats have larger decreases in extracellular HPC glucose levels during task training relative to those observed in young animals (Gold, 2005). In humans there is an age-related decrease in brain glucose uptake that exceeds that of oxygen use, resulting in loss of brain aerobic glycolysis (Goyal et al., 2017). These metabolic deficits in older adults are a likely contributor to cognitive impairments, as the ability to produce ATP declines by 8% per decade of life (Short et al., 2005), making aged individuals particularly vulnerable to metabolic alterations. Moreover, metabolic syndrome (Agrawal and Gomez-Pinilla, 2012) and insulin insensitivity are associated with cognitive deficits (for review, see Greenwood and Winocur, 2005). Together, these data indicate the strong association between metabolism and cognitive function.
While over consumption of an obesogenic high fat and high sugar diet leads to loss of dendritic spines in the PFC and perirhinal cortex, as well as to impairments in spontaneous object recognition tasks and set-shifting (Bocarsly et al., 2015), to date, very few studies have examined the ability of diet to enhance cognition and improve synaptic function. Ketogenic diets (KDs) are high in fat and low in carbohydrates, which leads to the production of fat-derived ketone bodies within the liver that enter the Krebs cycle for ATP production (Krebs, 1966; Egan and D’Agostino, 2016). The ability of these diets to bypass glucose/insulin signaling, which is compromised in old animals, suggests a potential utility in enhancing brain function across the lifespan. Previously, we have shown that 12 weeks of a KD can alter the expression of glucose and monocarboxylate transporters in the HPC, and reinstate expression of the vesicular glutamate transporter in old animals to the levels observed in young (Hernandez et al., 2018a)."