Low Levels of Manganese Type of SOD Through Out Life Increases Cancer Risk Dramatically

October 25, 2004

Mice were bred to have life-long low levels of manganese-SOD, with 50% less SOD activity in all tissues throughout life. These mice had elevated oxidative damage. The DNA in their chromosomes, referred to as nuclear-DNA had increased damage versus normal mice. The levels of nuclear-DNA damage increased with age and at 26 months was significantly higher than normal mice, with a 15% increased damage to nuclear-DNA in the heart and greater than 60% damage to the nuclear-DNA in the liver. Mitochondrial-DNA was also more damaged in tissues including the liver and brain. This increased oxidative damage to the DNA is associated with a 100% risk of developing cancer). The study appears in the December 2003 issue of the journal Physiological Genomics.

Commentary by Jerry Hickey, R.Ph.

The DNA within the chromosome in the nucleus of the cell is more effectively protected than the DNA in the mitochondria of the cell. Lacking Superoxide Dismutase decreased the ability to protect this genetic material. If an important part of the DNA within the chromosome is damaged, such as a tumor suppressing gene, the DNA can encode copies of this mutated version of itself allowing the formation of a cancerous tumor. When you supplement with an orally absorbable form of Superoxide Dismutase it couples with three different minerals, manganese, copper, and zinc. Depending on the tissue, the appropriate combination of SOD and its mineral protect this tissue. The combination that protects the DNA is the manganese combination.

Resveratrol and Propolis Fight Late Stage Prostate Cancer

The nutrients Resveratrol and Propolis were tested on androgen-resistant prostate cancer; this resembles the last stage of prostate cancer. Both nutrients caused the cancer cells to die from multiple causes. The study is published in a recent issue of the journal Oncology Research 2004;14(9):415-26.

The Role of Chempreventive Agents in Cancer Therapy

The formation of a cancerous tumor is a multi-step process triggered by carcinogens (cancer causing substances, e.g. tobacco, radiation, pollutants). Extensive research in the last few years has revealed that regular consumption of certain fruits and vegetables can decrease the risk of acquiring specific cancers. Phytochemicals derived from these fruits and vegetables are referred to as chemopreventive agents (nutrients that decrease the risk of cancer). They include Genestein (from soybeans), Resveratrol (from red wine), Diallyl sulfide and S-Allyl Cysteine (from garlic especially when aged), Allicin (from fresh garlic), Lycopene (from tomato oleoresin), Capsaicin (from cayenne peppers), Curcumin (Turmeric), 6-Gingerol (from ginger), Ellagic Acid (from berries and pomegranate), Ursolic Acid (from loquat), Silymarin (from milk thistle), Anethol (from anise and fennel), Catechins (from green tea, apple skins, red wine, and garlic), and Eugenol (from cloves).

These agents have been shown to suppress the proliferation of cancer cells (proliferation is the increase in number of cancer cells due to uncontrolled growth and cell division). They inhibit the effects of growth factors, inhibiting the growth and maturing of cancer cells. They induce the otherwise immortal cancer cells into committing cellular suicide. They short circuit the cancer process by inhibiting cancer associated enzymes and proteins. They inhibit the ability of cancer cells to create their own blood supply and routes of nourishment. They inhibit cancer causing cellular inflammatory mediators. They may have untapped therapeutic value.

These chemopreventive agents also very recently have been found to reverse the ability of cancerous tumors to shield themselves from the effects of chemotherapy and radiation in patients undergoing cancer treatment. Thus these chemopreventive agents have potential to be used as adjuncts to current cancer therapies. The report as formulated at the Comprehensive Cancer Center, Our Lady of Mercy Medical Center, New York Medical College, Bronx, New York. The study is published in the November 25th issue of Cancer Letters.

Commentary by Jerry Hickey, R.Ph.

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The study appears in the November 25th, 2004 issue of Cancer Letters.