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| Flavonoids are being evaluated by themselves, and together with other substances, in the treatment of cancer. A synthetic relative of bioflavonoids, flavone acetic acid (FAA), is an immune booster, although not a very useful drug by itself. FAA increases natural killer-cell activity in mice. In Italian laboratory tests, FAA produced mixed results. Some transplanted human tumors were unaffected, but those grown under the skin and in the liver of test animals were significantly inhibited. Italian scientists said this test demonstrated the "great importance of the site of tumor growth for FAA efficacy." 90 |
| FAA was also clinically evaluated in cancer patients. Fifty-four patients were given large infusions for up to six hours. No objective responses were seen in this trial, however. Scientists are puzzling over why this drug works much better in mice than in people. Some have concluded that there is "a clear immunological component in the mechanism of action of FAA."91,92 |
| However, FAA does seem to have one powerful effect. When FAA is combined with interleukin-2 (IL-2), the combination is very powerful. As an added benefit, IL-2 taken with FAA does not have its usual severe toxicity. In mice, kidney cancer treated with FAA and IL-2 resulted in "up to 80 percent long-term survival" whereas either substance alone was "unable to induce any long-term survivors." The two substances appeared to work by stimulating natural killer-cells and the production of natural tumor-necrosis factor. Used together in humans, there were nearly 60 percent more long-term survivors than when either drug was used alone.93 9495 |
| Because flavonoids inhibit carcinogenesis by several mechanisms, my protocols always include flavonoid supplements, usually more than one, and in fairly high doses; for example, POCs: 100 to 200 mg two to six times daily or quercetin: 500 to 1,000 mg three times daily. |
| The Anticancer Actions of Flavonoids |
| Flavonoids have the following anticancer actions: |
| 1. Inhibition of mitosis. They reduce the rate of uncontrolled cell division caused by cancer. |
| 2. Blocking or competing for cell-surface receptor sites. By occupying these receptor sites, cancer-cell-surface enzymes have nowhere to dock on the surface of healthy cells and therefore cannot transform healthy cells. |
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