I think another mechanism that may be in play here, with Dr. Stephens' system, is suppression of hyperglycolysis. Which produces only pyruvate and a little CO2 and energy, and burdens the brain. The brain responds by diminishing consumption of glucose and switching partially to using glutamine. This is EXACTLY what happens with Warburg's "cancer field" idea.
I proposed this idea to ChatGPT
Potential Mechanisms for Glucose Loading to Work:
Potential Mechanisms for Glucose Loading to Work:
• Enhancing Mitochondrial Function: By providing ample glucose,
you could support mitochondrial oxidative metabolism by ensuring a
steady supply of pyruvate to the Krebs cycle, increasing electron
transport chain activity and ATP production.
• Reducing Lactate Buildup: Slowing down glycolysis might reduce the accumulation of
lactate (which occurs when pyruvate is converted to lactate in
anaerobic glycolysis), which is often a hallmark of hyperglycolysis
in conditions like cancer or impaired mitochondrial function.
• Rebalancing ATP Production: Encouraging ox-phos would lead to
more efficient ATP production (since oxidative phosphorylation
produces significantly more ATP per glucose molecule than
glycolysis) and may reduce the compensatory need for rapid
glycolysis in states of high energy demand.
Caveats:
• Cancer Cells and Adaptation: In cancer, cells have adapted to
rely on glycolysis due to changes in mitochondrial function or other
oncogenic signaling. Glucose loading alone may not be enough to
reverse these metabolic shifts. However, in non-cancerous
hyperglycolytic states, it could potentially restore metabolic
balance.
• Tumor Environment: The tumor microenvironment, which
often includes hypoxia (low oxygen), favors glycolysis. Simply
providing more glucose may not necessarily shift cells back to
ox-phos in such environments without other interventions (e.g.,
improving oxygen availability or mitochondrial function).
Conclusion:
While it is speculative, the concept of glucose loading could
theoretically help regulate metabolism by reducing hyperglycolysis and
encouraging oxidative phosphorylation, leading to increased CO₂
production and more efficient energy use. This could be beneficial in
certain cases of metabolic dysregulation, though in cancer cells, their
preference for glycolysis may make this strategy more complex. Further
research would be needed to confirm whether this approach is effective
across different conditions where hyperglycolysis occurs.