Nutritional Ketosis -Implications for Mitochondrial Function & Human Health.
Once mitochondrial functionality has diminished an excessive production of reactive oxygen species (ROS) occurs and an onset of etiology of many chronic diseases, such as cardiovascular disease, diabetes, neurodegenerative disorders, and cancer. Moderate levels of mitochondrial ROS, however, can protect against chronic disease by inducing upregulation of mitochondrial capacity and endogenous antioxidant defense. Homeostatic occurrence is vital and functionality of mitohormesis, is present where increased reliance on mitochondrial respiration, which occurs through diet or exercise. Nutritional ketosis is a safe and physiological metabolic state induced through a ketogenic diet low in carbohydrate and moderate in protein. This serves an an adjunct to increase mitochondria functionality.
Such a diet increases reliance on mitochondrial respiration and may, therefore, induce mitohormesis. The ketone β-hydroxybutyrate (BHB) found in GoKeto and MCT similar to nutritional ketosis, to levels resulting from fasting, acts as a signaling molecule in addition to its traditionally known role as an energy substrate. BHB signaling induces adaptations similar to mitohormesis, thereby expanding the potential benefit of nutritional ketosis beyond carbohydrate restriction. This review describes the evidence supporting enhancement of mitochondrial function and endogenous antioxidant defense in response to nutritional ketosis, as well as the potential mechanisms leading to these adaptations.
Ketogenic diet promotes autophagy: ketone generation requires autophagy.