Cancer

 

Dietary Ketosis In
The Treatment of Solid Tissue Malignancy

Dr. Dana Myatt

 “Attack by stratagem: hence, to fight and conquer in all your battles is not supreme excellence;
supreme excellence consists in breaking the enemy’s resistance without fighting.”
—Sun Tzu, “The Art of War”

Many believe that cancer cells, damaged by mutation, are more resilient than normal cells. However, malignant cells are largely incapable of the metabolic flexibility displayed by normal cells, and therein lies their weakness and the potential for a gentle but highly effective point of attack.

Nutritional and botanical factors can have profound positive effects in cancer treatment, but the single most potent anti-cancer strategy documented in the medical literature strikes at the core of cancer’s metabolism: glycolysis, especially anaerobic glycolysis, and impaired mitochondrial function.

Numerous animal and human studies have demonstrated that the glycolytic pathway of cancer cells can be confounded by dietary-induced ketosis, often with profound apoptotic effects on cancer cells but without negative consequence — and in fact with protective effects — to normal cells.(1-6) Metabolic ketosis curtails cancer growth by a variety of mechanisms including:

  1. Decreasing the glucose substrate required for cancer cell metabolism. Most tumors express abnormalities in the number and function of their mitochondria. (7-12) Such abnormalities prevent the bioenergetic utilization of ketone bodies, which require functional mitochondria for their oxidation.
  2. Decreasing insulin, a secondary growth factor for cancer cells. (13-14)
  3. Decreasing inflammation. Inflammation acts to promote cancer by altering cell-to-cell communication and delaying local detoxification.(15-25) Metabolic ketosis has significant anti-inflammatory effects. (9, 26-29)
  4. Decreasing ROS production. Reactive Oxygen Species are known to promote cancer (30-33); metabolic ketosis decreases ROS production. (34-37)
  5. Reversing cachexia while simultaneously decreasing tumor weight. (38-40)
  6. Decreasing angiogenesis. (29, 41-42)
  7. Inducing apoptosis. (11,29,38)
  8. Suppressing the p53 oncogene, the most common point mutation observed in human cancer; more than 50% of all human tumors examined to date have identifiable p53 gene point mutations or deletions. A ketogenic diet has been shown to suppress the p53 oncogene in animal models. (43)
  9. Acting synergistically with chemotherapy and/or specific nutritional supplementation. (44-45)

In spite of improved availability of foods containing anti-carcinogenic phytonutrients and vitamins, most types of cancer have not declined as expected. This correlates to the overall calorie increase and overweight condition of our society, a condition which puts us in “constant feast” mode instead of the periodic fasting our ancestors previously experienced. (46) Some observers feel that our previous occasional fasts, which would induce ketosis, were beneficial for cancer control. It has also been hypothesized that alternative “cancer diets” such as juice fasting, calorie restriction or the use of Coley’s toxins are effective primarily because they induce metabolic ketosis.

This presentation will serve as a review of the behavior and biochemistry of cancer cells common to all solid tissue malignancies and present a novel but well-documented clinical nutritional strategy which targets multiple cancer cell vulnerabilities while simultaneously protecting the function of normal cells and tissue.

References:

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