Table sugar or 50% fructose is harmful to the cell metabolism. It pushes metabolic syndrome effects and has the opposite effect of fat burning beta hydroxybutyrate.
The obvious question is how much suppression of beta hydroxybutyrate and starvation gene transcription is prevented?
Can 12 hours of daily fasting, exercise and their mimetics like Ursolic acid recover starvation gene expression and restore cellular metabolic health?
I think every debt can be paid, every sin forgiven with the penance of 12 hours of beta hydroxybutyrate augmented recovery.
I further conjecture that young cells that are metabolically healthy are more resilient and recover easier in the same way a young adult with good health recovers faster from pneumonia compared to an older adult.
Action: limit fructose and maximize beta hydroxybutyrate in your daily cycle. Remember that debt can be paid for health maintenance. It is also true that resilience or health building is when debts are less than income, costs less than capital reserves. The evidence of healthy reserves is fidelity of cellular genetic code, stable telomere length, reduced markers of inflammasome activity, increased numbers of mitochondria producing manageable ROS levels and effective cell quality control activities like autophagy and mitophagy.
Dietary fructose aggravates the pathobiology of traumatic brain injury by influencing energy homeostasis and plasticity
Fructose consumption has been on the rise for the last two decades and is starting to be recognized as being responsible for metabolic diseases. Metabolic disorders pose a particular threat for brain conditions characterized by energy dysfunction, such as traumatic brain injury. Traumatic brain injury patients experience sudden abnormalities in the control of brain metabolism and cognitive function, which may worsen the prospect of brain plasticity and function. The mechanisms involved are poorly understood. Here we report that fructose consumption disrupts hippocampal energy homeostasis as evidenced by a decline in functional mitochondria bioenergetics (oxygen consumption rate and cytochrome C oxidase activity) and an aggravation of the effects of traumatic brain injury on molecular systems engaged in cell energy homeostasis (sirtuin 1, peroxisome proliferator-activated receptor gamma coactivator-1alpha) and synaptic plasticity (brain-derived neurotrophic factor, tropomyosin receptor kinase B, cyclic adenosine monophosphate response element binding, synaptophysin signaling). Fructose also worsened the effects of traumatic brain injury on spatial memory, which disruption was associated with a decrease in hippocampal insulin receptor signaling. Additionally, fructose consumption and traumatic brain injury promoted plasma membrane lipid peroxidation, measured by elevated protein and phenotypic expression of 4-hydroxynonenal. These data imply that high fructose consumption exacerbates the pathology of brain trauma by further disrupting energy metabolism and brain plasticity, highlighting the impact of diet on the resilience to neurological disorders.
