CURCUMIN
A potent antioxidant with specific antiviral, anti-inflammatory, anti-cancer and cholesterol-lowering effects
Curcumin is especially recommended for hepatitis C patients. One study found it to be more effective than green tea extract in suppressing viral damage to liver cells. Curcumin induces cancer cell apoptosis. Apoptosis can be defined simply as programmed cancer cell death. Cancer researchers are focusing in on agents that induce apoptosis as the next generation of cancer drugs. Many of the nutrients in the cancer treatment protocol such as selenium, vitamin A, green tea and vitamin D3 induce apoptosis.
The most effective nutrient available to induce apoptosis may be curcumin. Curcumin is an antioxidant extract from the spice turmeric that produces a wide range of health benefits. Cancer patients should be taking 2000 mg to 4000 mg a day of curcumin extract with a heavy meal. In a wide range of cancer cells, curcumin has been shown to induce cell shrinkage, chromatin condensation, DNA fragmentation and block cellular signal transduction, all of which are characteristics of apoptosis according to an article published in the journal Nutrition and Cancer USA (26/1 1996).
Full source: BRITISH JOURNAL OF PHARMACOLOGY, 2000, Vol 129, Iss 2, pp 231-234
A study investigated the effect of curcumin on artificially induced kidney disease in rats. Results indicated that treatment with curcumin prevented the kidney injury and restored kidney function. Treatment with curcumin significantly protected against proteinuria, albuminuria, hypoalbuminaemia and hyperlipidaemia. Curcumin inhibited the increase in urinary excretion of N-acetyl-beta-D-glucosaminidase (a marker of kidney tubular injury), fibronectin and glycosaminoglycan and blood cholesterol. The data also demonstrated that curcumin protected against kidney injury by suppressing free radicals and increasing kidney glutathione content and glutathione peroxidase activity (endogenous antioxidants). Curcumin also eliminated kidney microsomal and mitochondrial lipid peroxidation. The data suggest that administration of curcumin is a promising approach in the treatment of kidney disease.
References:
1. On tumor cells in a lab dish, curcumin prevents or slows prostate and lung cancer. But dietary consumption of turmeric, researchers report, so far shows no effect on those organs and failed to inhibit tobacco-induced tumors (Cancer Lett 1999 Apr 1;137(2):123-30).
2. Recent studies have found that curcumin has a dose-dependent chemo-preventive effect in rats during promotion/progression stages of colon cancer (Cancer Res 1999 Feb 1; 59(3): 597-601). It has similar preventive effects against skin cancer, oral cancer and forestomach and other intestinal tumors (J Surg Res 2000 Apr; 89(2): 169-75).
3. According to Tufts researchers, "a mixture of curcumin and isoflavonoids is the most potent inhibitor against the growth of human breast tumor cells. These data suggest that combinations of natural plant compounds may have preventive and therapeutic applications against the growth of breast tumors induced by environmental estrogens" (Environ Health Perspect 1998 Dec;106(12):807-12)
4. Turmeric compares with soy, licorice, red clover, and thyme in binding to progestrone and estrogen receptors in breast cancer cells (Proc Soc Exp Biol Med 1998 Mar;217(3):369-78).
4. Kentucky researchers found that curcumin "inhibited proliferation of a variety of B lymphoma cells" (Clin Immunol 1999 Nov;93(2):152-61).
5. Curcumin may or may not protect against cellular damage from radiation, perhaps depending on dose. It appears to protect against damage to certain organs brought about by some chemotherapy agents. In hamsters it protects the kidneys from Adriamycin (Br J Pharmacol 2000 Jan;129(2):231-4). If you are taking radiation or chemotherapy, discuss your diet and use of any antioxidants with your oncologist.
6. Typical dietary amounts of turmeric have an anti-oxidant effect that protects rats from cataracts (Toxicol Lett 2000 Jun 5;115(3):195-204).
7. Curcumin protects rats from liver-damage caused by toxins (J Pharm Pharmacol 2000 Apr; 52(4): 437-40; Carcinogenesis 2000 Feb; 21(2): 331-5)