Dominic D’Agostino is a renowned researcher with a keen interest in conducting ketone research, particularly on keto nutrition, ketone supplementation, and ketone ester. Also, in the course of his career, Dom D’Agostino has co-hosted several conferences on ketone bodies, ketone technologies and various other metabolic-based therapies centered around keto-nutrition.
Our cognitive capacity and resilience are important for not only daily consciousness and self-independence, but also relationships and brain health optimization. Cognitive skills are developed in early infancy as a component of maturing neurodevelopmental processes. Regrettably, retrograde alterations can happen during physiological aging. Various nutritional and dietary strategies provide viable cures for cognitive decline and preservation of cognitive capacity.
Following ketone production in the liver, or via ketone supplementation (e.g. KetoStart), peripheral tissues receive ketones for fuel and metabolic-associated signaling. The body typically employs ketones as an alternative fuel source, usually when glucose is scarce. With various techniques that partially imitate hunger and carbohydrate depletion, ketones can be purposefully elevated in the blood and biologically produced to boost physiological levels that can further enhance brain energy metabolism.
Consequently, ketone bodies support cognitive functions by contributing to the brain's bioenergetic capacity, and through signaling roles associated with suppression of neuroinflammation. Since metabolic bioenergy is one of the targets of drug models intended to treat cognitive diseases, the importance of ketone bodies to the brain cannot be over-emphasized.
Although glucose is the primary biofuel source that the body produces, aging cells or disease may impair the breakdown of glucose in the brain. Ketone bodies can effectively provide the fuel that might supplement the defective glycolytic metabolism, which consequently improves cognitive health and stops disease progression.
According to in vitro studies, ketones actively guard neurons against hypoglycemia-induced mortality and various environmental toxins too. This effect is possibly caused by both an increase in mitochondrial ATP production and a decrease in ROS production. The ketone body beta-hydroxybutyrate (BHB) can replace glucose in hypoglycemia situations, retaining metabolic activity, avoiding peroxidation, and impairing neuronal death. This has been demonstrated in both in vivo and in vitro research. This defense may be linked to the impact that ketone-induced autophagy has on cells and is one of the key features associated with the many cellular and molecular protective roles that nutritional or supplemental ketosis has on people using this longevity strategy. For more information on this topic and more see KetoNutrition.org website.
