What specifically, constitutes a metabolic therapy, as pertains to cancer?
Focusing on the novel means of energy production in a tumor cell offers a cogent point of departure for grasping the essentials of both why and how a metabolic therapy would constitute a clinically viable means of controlling disease.
Of particular interest would be to understand the precise process by which a tumor cell can become cancerous.
To this end, an appreciation that multiple vectors of insult to regular mitochondrial energy production can offer insight into this phenomenon, given that intermittent hypoxia, viruses, bacteria, carcinogens, toxins, and genetic abnormalities, can all contribute towards damaging the number, structure and function of mitochondria, such that, over time, cells that don’t die as a result of these insults can come to rely on an ancient fermentation pathway for energy production, relying primarily on the carbohydrate glucose and the amino acid glutamine to drive ATP synthesis.
Hence, it is at this point that the punchline begins to reveal itself. If tumor cells, unable to oxidize fatty acids for energy, and unable to produce meaningful amounts of energy from other metabolites, must almost exclusively rely on glucose and glutamine for energy production, then consistent control of glucose and glutamine would determinatively impugn tumor viability, while sparing normal tissue.
Therefore, the combinatorial use of glucose control via the precise administration of macronutrients and calories as a means of moving glucose consistently within or close to a therapeutic range of 55-65mg/dL (3.0-3.5mMol/L), concurrent to an elevation in ketone bodies within the 4-7mMol/L range, limits substrate availability of glucose to disease.
These effects can be further enhanced via the use of novel drugs, such as 2-Deoxyglucose, which act as an inhibitor of glycolysis given that in fact while 2DG is in fact a glucose molecule, though interestingly, it has a hydrogen at the carbon 2 position instead of a hydroxyl group, and as such, is unable to complete the glycolysis process, failing to produce net ATPs.
Attendantly, intermittent use of pan-glutamic inhibitors such as 6-Diazo-5-Oxo-L-Norleucine, further marginalize tumor energy production by inhibiting the suite of enzymes which catalyze glutaminolysis.
Furthermore, concurrent and overlapping use of Hyperbaric Oxygen Therapy which is directly cytotoxic to tumor cells as a result of acutely and massively upregulating Reactive Oxygen Species, along with the use of repurposed drugs such as Mebendazole, which inhibits the formation of microtubules thereby inhibiting mitosis and functioning as an antiproliferative, combine to sustainably and non-toxically manage disease.