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Life Extension Magazine

LE Magazine February 2003

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Anti-Cancer Foods and Supplements

Soy

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Soybeans contain several types of cancer-fighting phytochemicals. Soy isoflavones are non-steroidal plant compounds that block hormone-related cancers. These so-called "phytoestrogens" actually block estrogen from getting into cells, and prevent hormone-related cancers including prostate and breast cancer. In addition to their hormone-blocking effects, they also have powerful antioxidant activity.

In a large study, men who drank soy milk more than once a day had a 70% reduced rate of prostate cancer. A similar study on women shows that a soy-based diet, including 36 oz. of soymilk a day (113 to 207 mg/day of total isoflavones) reduced levels of 17-estradiol (strong estrogen) by 25%.

Soy isoflavones may protect against bladder cancer. In a recent study, genistein inhibited the growth of eight different types of human bladder cancer cells. Daidzein and other isoflavones caused the cells to self-destruct.

New research shows that phytoestrogens, including soy phytoestrogens, shut down the activation of the estrogen receptor. This receptor is provoked into sending "grow" signals when it encounters chemical estrogens or estradiol (strong estrogen). In other words, people with hormone-related cancers have too many estrogen "doorways" on their cells. This results in a flood of strong estrogen into the cell. This type of estrogen activates proliferation of the cell. Normal cells have far fewer estrogen receptors. Normal cells also have an equal number of a related receptor that phytoestrogens fit into and activate. Cancer cells are missing this phytoestrogen receptor. The phytoestrogen receptor acts as a counterbalance on the estrogen receptor, preventing it from causing growth.

Tea

During the colonial era, most of North America was owned by a monopoly called the East India Company. When the British government, acting on behalf of the monopoly, granted it the exclusive right to sell tea in America, forcing all other merchants out of business, the colonists rebelled. The Boston Tea Party was the opening act of the American Revolution. It's a testament to the power of tea that it was instrumental in creating America. Tea has been used as medicine since at least the Shang dynasty (1766-1122 B.C.).

Modern research confirms that tea has health benefits, notably anti-cancer properties. Most of this research has been done with green tea (which is minimally oxidized), rather than other teas such as black tea. Tea contains several different phytochemicals, including epigallocatechin-3-gallate (EGCG), a polyphenol with proven biochemical actions against cancer. Tea also contains vitamins A , C and E, a unique amino acid known as theanine, carotene, zinc and many other cancer fighting substances.

One of the most striking studies on green tea was done by a group of Japanese researchers on women who had been treated for breast cancer. Analysis six years later of women with stage I or II breast cancer showed that those who drank five or more cups of green tea a day slashed their risk of recurrence almost in half. This is equivalent to approximately 200 to 400 mg of EGCG. Furthermore, the researchers found that the more green tea a woman drank before she got cancer, the fewer metastases to lymph nodes she would have (if she was premenopausal). Women who engage in the Japanese tea ceremony are half as likely to die not only from breast cancer but from any cause, according to researchers who followed them for eight years.

Two new studies show that green tea or EGCG inhibits certain types of leukemia. When cells from adults with T-cell leukemia are treated with green tea polyphenols or EGCG, the cancer stops multiplying. Similarly, when various types of leukemia cells are treated with EGCG, they self-destruct. According to the study's authors, "Besides anticarcinogenic activity, EGCG is expected to have a new function for leukemia therapy without side effects" (referring to EGCG's ability to make existing cancer cells stop growing).

I3C

Indole-3-carbinol stands alone as the most well-studied natural estrogen modulator. Found in cruciferous vegetables such as cabbage, cauliflower and broccoli, I3C has proven effects against hormone-related cancers.

I3C may be an important tool against environmentally-caused cancer because it can block dioxin from entering cells. Dioxin is a chlorine chemical, known as the most toxic chemical ever created-so toxic it is measured in parts per trillion. The main source of it for most people is meat and dairy products. Popular fast foods such as McDonald's Big Macs® have been found to contain metabolites of dioxin. Dioxin is suspected as a cause (or contributing cause) of breast, prostate, lymphoma and lung cancers.

I3C comes to the rescue by its ability to compete with dioxin for entry into cells. The same receptors, or doorways, that allow estrogen and dioxin into cells, allow I3C as well. When I3C and dioxin are put together with cells, I3C keeps some of the dioxin out by physically blocking the harmful chlorine chemical. This same mechanism also protects cells from strong estrogen that can promote cancer growth.

A recent study shows that treatment with I3C can reverse precancerous conditions of the cervix in humans. I3C may also protect smokers. When I3C was given to rats forced to ingest smoke, DNA damage was reduced over 50% in lungs and trachea, and 65% in the bladder. It also inhibits heterocyclic amines, dangerous carcinogens that form when meat is cooked. One study showed that I3C was up to 95% effective in inhibiting carcinogens. (Note: the recommended dose for I3C is 400 mg for most women and 600 mg for most men, depending on weight).

Zinc

Zinc is crucial for immunity. Thirty days of suboptimal zinc intake causes a 30% to 80% loss of immune defense. Studies show that zinc is important for natural killer (NK) cells to multiply and function. NK cells are the body's first-line defense against certain types of cancer. Supplemental zinc has been shown to increase antibody response and T-cell counts. Zinc deficiency causes the thymus to atrophy: supplements can reverse this.

Think Prevention

Cancer is the second leading cause of death in America. The time to think about prevention is now. Eliminating chemical exposure (yard sprays, household cleaners, paint, plastic, etc.) as much a possible reduces risk. Changing from a meat-based diet to plant-based food can slash risk by as much as 50%. Certain types of supplements can further reduce risk by terminating cancer before it has a chance to grow and spread.

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Zinc status is very much related to infection and disease. People with lymphoma have decreased levels of zinc and increased levels of copper. This trend reverses during remission. Zinc deficiency is prevalent in alcoholism, gastrointestinal disorders and renal disease. Infections appear to reduce zinc levels. And reduced zinc levels appear to increase the chances of getting an infection.

It's impossible to make a blanket recommendation about how much zinc a person should take. Too much zinc is as bad as too little. Too much zinc depresses immunity as surely as too little. Very little research has been done on zinc, and unfortunately, "There is no universally accepted single measure suitable to accurately assess the zinc status of an individual."* Currently, 30 to 50 mg of elemental zinc per day is the recommended amount. However, this is very arbitrary inasmuch as an individual might need different amounts of zinc at different times, depending on their health, age, diet and other factors that affect zinc utilization, absorption and acquisition. As an example of how difficult pinpointing zinc supplementation can be, a study on healthy men showed that 300 mg/day of elemental zinc suppressed immunity. Yet, a study in people over age 70 found that 440 mg of zinc a day significantly increased immunity. One approach is to look at copper levels instead. If copper levels are elevated, or the copper-to-zinc ratio is high, zinc should be taken until the balance normalizes, regardless of whether lab results fall within the "normal" range.

Anti-inflammatories

Non-steroidal anti-inflammatory drugs (NSAIDs) exploded on the scene in 2000 as possible cancer preventive agents. The latest research indicates that NSAIDs, including aspirin, have multiple and diverse actions against the growth and mestastasis of cancer cells. Colon cancer has received the most attention. Risk can be slashed 50% by the long-term use of NSAIDs such as ibuprofen. Esophageal, stomach, rectal and bladder cancer risk are also significantly reduced. For breast cancer, 2 to 10 years of NSAIDs reduces overall risk, and reduces the risk of metastases everywhere except nearby lymph nodes.

Aspirin may also reduce risk, but apparently in a different way, and not as strongly. When researchers at the University of Leeds tested aspirin on colon cancer cell lines, it stopped the cells from growing but did not induce apoptosis (cell death). The same cells treated with the NSAID drug indomethacin were growth-arrested and destroyed by apoptosis. Different NSAIDs work differently against cancer cells, and it may turn out that some work better for some types of cancers than others. Combining aspirin with an NSAID may enhance the effectiveness.

The natural anti-inflammatory, curcumin, has demonstrated similar and powerful effects against the growth of cancer cells. Some new concerns have been raised about the expensive and highly advertised NSAIDs, Celebrex and Vioxx drugs. According to the drug reference book Worst Pills, Best Pills, they may have previously unknown gastrointestinal and cardiovascular side-effects. The manufacturers of both drugs have been warned by the FDA to cease misrepresenting their safety and effectiveness.

One of the interesting properties about anti-inflammatories is that they may conserve the body's antioxidants, particularly the carotenoids. In a study from the UK, 1200 mg/day of ibuprofen helped cancer patients recover their levels of beta-carotene, lutein and lycopene. This phenomenon can be explained by the fact that inflammatory reactions generate free radicals that deplete the body of such plant-derived antioxidants. Anything that suppresses inflammation, be it ibuprofen, fish oil or curcumin, conserves precious antioxidants in the body. Chronic inflammation is related to increased cancer risk, and inflammation enhances the ability of cancer to spread.

Supplements versus food

Food contains all the nutrients the human body needs. And if we eat the right kind of food, we'll get them. The problem is we don't. Some of us, however, are chasing our hot dogs with vitamins in an effort to fortify our diets. That's the approach of the industry that makes food products-they fortify their products with vitamins. It's not the greatest approach, but it's not altogether bad. Vitamins can undo some of our bad habits. They can't replace good diet, but they can have a beneficial effect.

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And in fact, sometimes a supplement gets the job done better than a food containing it. The reason is partly due to bioavailability. Bioavailability has to do with the body's ability to utilize a nutrient. The vitamins in food are attached to proteins. They must be separated from those proteins in order to be utilized. Different factors can conspire to impede that process. For example, phytic acid that is found in the hulls of grains like wheat can interfere with the body's absorption of zinc and calcium. Another classic example is the necessity of a stomach chemical known as intrinsic factor for vitamin B12 utilization. And then there's the problem of how various things a person eats interact. A person who dresses their salad with non-fat dressing will not be able to utilize the vitamin K in the leaves of the lettuce: fat must be present for the vitamin to be absorbed. Supplements avoid these problems. Vitamin K supplements, for example, come ready-made with a drop of oil for absorption. The bioavailability problem has been demonstrated in studies showing that if Indonesian women eat a beta-carotene-fortified cracker, more beta-carotene and vitamin A will appear in their blood than if they eat stir-fried vegetables containing beta-carotene.

Folate is another vitamin that seems more bioavailable as a supplement. Research in the UK shows that "intake of folic acid supplements provides a greater elevation in serum folate levels than dietary food intake, suggesting that dietary manipulation is an ineffective strategy (for pregnant women)." This agrees with data from the Nurses' Health Study where folate from food lowered the risk of colon cancer a little, but supplemental folate lowered it significantly.

This highlights one of the other benefits of supplements. They are concentrated and you know how much you're getting (if the supplement is from a reputable company). One of the problems with trying to get enough cancer-fighting nutrients from food is that the sheer amount of vegetables and fruit a person has to consume is daunting if the person wants to get a full spectrum of protection, not just avoid deficiency disease. For example, if a person wanted to cover all the carotenoids every day, they would need to eat green, yellow, orange and red vegetables-all of them. Let's say they also wanted the benefits of I3C (indole-3-carbinol), a phytochemical in cruciferous vegetables, they would have to add cabbage, broccoli, cauliflower or mustard. If they also wanted to cover the citrus flavonoid spectrum, they would also have to eat a wide variety of citrus fruit-and so on. If a person wants to ingest a wide variety of anti-cancer compounds on a daily basis, in a substantial amount, it's more practical to take them in a concentrated form. A person can hold in one hand vitamins found in bushels of vegetables, pounds of soy and mountains of fruit. However, supplements should not replace a good diet. Whole foods contain important and diverse factors that maintain health, and everyone should be eating as much of them as possible. Supplemental vitamins can, however, provide an extra measure of protection. For cancer prevention, this is especially important.


References

Arif JM, et al. 2000. Inhibition of cigarette smoke-related DNA adducts in rat tissues by indole-3-carbinol. Mutat Res 452:11-18.

Bell MC, et al. 2000. Placebo-controlled trial of indole-3-carbinol in the treatment of CIN. Gynecol Oncol 78:123-9.

Bohlke K, et al. 1999. Vitamins A, C and E and the risk of breast cancer: results from a case-control study in Greece. Br J Cancer 79:23-9.

Bosetti C, et al. 2000. Fraction of prostate cancer incidence attributed to diet in Athens, Greece. Eur J Cancer Prev 9:119-23.

Caltagirone S, et al. 2000. Flavonoids apigenin and quercetin inhibit melanoma growth and metastic potential. Int J Cancer 87:595-600.

Chandra RK. 1984. Excessive intake of zinc impairs immune responses. JAMA 252:1443-6.
Chaumontet C, et al. 1997. Flavonoids (apigenin, tangeretin) counteract tumor promoter-induced inhibition of intercellular communication of rat liver epithelial cells. Cancer Lett 114:207-10.

"Do Not Use Celecoxib (CELEBREX) and Rofecoxib (VIOXX) for arthritis-the misnamed and overpriced 'super aspirins'". Worst Pills, Best Pills News. Washington, DC: April 2001; 27.
Dubois RN. 2000. Review article: cyclooxygenase-a target for colon cancer prevention. Alimet Pharmacol Ther 14 Suppl 1:64-7.

Duchateau J, et al. 1981. Beneficial effects of oral zinc supplementation on the immune resonse of old people. Am J Med 70:1001-4.

Egner PA, et al. 2001. Chlorophyllin intervention reduces aflatoxin-DNA adducts in individuals at high risk for liver cancer. Proc NY Acad Sci USA 98:14601-6.

Elkin AC, et al. 2000. Folic acid supplements are more effective than increased dietary folate intake in elevating serum folate levels. Br J Obstet Gynaecol 107:285-9.

Fong LY, et al. 1987. Zinc-deficiency and the development of malignant lymphoma in rats given a single intragastric dose of N-methyl-N-nitrosourea. IARC Sci Publ 84:261-3.
Fraker PJ, et al. the dynamic link between the integrity of the immune system and zinc status. J Nutr 130(5S Suppl):1399S-06S.

Gann PH, et al. 1999 Lower prostate cancer risk in men with elevated plasma lycopene levels: results of a prospective analysis. Cancer Res 59:1225-30.

Giovannucci E, et al. 1998. Multivitamin use, folate and colon cancer in women in the Nurses' Health Study. Ann Int Med 129:517-24.

Guengerich F, et al. 1991. Cytochrome P-450 oxidations and the generation of biologically reactive intermediates. Biological Reactive Intermediates IV, 1991, Plenum Press, New York.
Hatherill JR. Eat to Beat Cancer. Renaissance Books: Los Angeles. 1998.

Regenstein L. America the Poisoned. Acropolis Books Ltd.: Washington, DC. 1983.
Guyton KZ, et al. 1993. Oxidative mechanisms in carcinogenesis. British Med Bull 49:523-44.
He YH, et al. 2000. Indole-3-carbinol as a chemopreventive agent in 2-amino-l-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) carcinogenesis: inhibition of PhIP-DNA adduct formation, acceleration of PhIP metabolism, and induction of cytochrome P450 in female F344 rats. Food Chem Toxicol 38:15-23.

Holland MB, et al. 1995. Estrone-induced cell proliferation and differentiation in the mammary gland of the female Noble rat. Carcinogenesis 16:1955-61.

Hsu JT, et al. 2000. Regulation of inducible nitric oxide synthetase by dietary phytoestrogen in MCF-7 human mammary cancer cells. Reprod Nutr Dev 40:11-18.

Jacobsen BK, et al. 1998. Does high soy milk intake reduce prostate cancer incidence? The Adventist Health Study (United States) [see comments]. Cancer Causes Control 9:553-7.
Jin Z, et al. 2002. Soy isoflavones increase latency of spontaneou mammary tumors in mice. J Nutr 132:3186-90.

Johnson PW, et al. 1987. Enhanced lytic susceptibility of Ha-ras transformants after oncogene induction is specific to activated NK cells. J Immunol 138:3996-03.
Kawaii S, et al. 1999. HL-60 differentiating activity and flavonoid content of the readily extractable fraction prepared from citrus juices. J Agric Food Chem 47:128-35.
Kawaii S, et al. 1999. Antiproliferative activity of flavonoids on several cancer cell lines. Biosci Biotechnol Biochem 63:896-9.

Liang Y, et al. Suppression of inducible cyclooxygenase and inducible nitric oxide synthase by apigenin and related flavonoids in mouse macrophages. Carcinogenesis 20:1945-52.
Li HC, et al. 2000. Green tea polyphenols induce apoptosis in vitro in peripheral blood T lymphocytes of adult T-cell leukemia patients. Jpn J Cancer Res 91:34-40.
Lu LJ, et al. 2000. Decreased ovarian hormones during a soya diet: implications for breast cancer prevention. Cancer Res 60:4112-21.

Mäkelä S, et al. 1998. Inhibition of 17 -hydroxysteroid oxireductase by flavonoids in breast and prostate cancer cells. Proc Soc Exp Biol Med 217:310-16.

McMillan DC, et al. 2000. Changes in micronutrient concentrations following anti-inflammatory treatment in patients with gastrointestinal cancer. Nutr 16:425-8.

Michaud DS, et al. 2000. Intake of specific carotenoids and risk of lung cancer in 2 prospective US cohorts [see comments]. Am J Clin Nutr 72:990-97.
Mills PK, et al. 1989. Cohort study of diet, lifestyle and prostate cancer in Adventist men. Cancer 64:598-04.

Miodini P, et al. 1999. The two phyto-estrogens genistein and quercetin exert different efects on oestrogen receptor function. Br J Cancer 1150-55.

Nakachi K, et al. 1998. Influence of drinking green tea onbreast cancer malignancy among Japanese patients. Jpn J Cancer Res 89:254-61.

Noroozi M, et al. 1998. Effects of flavonoids and vitamin C on oxidative DNA damage to human lymphocytes. Am J Clin Nutr 67:1210-17.

Ong T, et al. 1989. Comparative antimutagencity of 5 compounds against 5 mutagenic complex mixtures in Salmonella typhimurium strain TA98. Mutat Res 222:19-25.
Otsuka T, et al. 1998. Growth inhibition of leukemic cells by (-)-epigallocatechin gallate, the main constituent of green tea. Life Sci 63:1397-403.

Parazzini F, et al. 2000. Population attributable risk for ovarian cancer. Eur J Cancer 36:520-4.
Porrini M. et al. 2000. Lymphocyte lycopene concentration and DNA protection from oxidative damage is increased in women after a hort period of tomato consumption. J Nutr 130:189-92.
Post JFM, et al. 1992. Growth inhibitory effects of bioflavonoids and related compounds on human leukemic CEM-C1 and CEM-C7 cells. Cancer Lett 67:207-13.

Reddy KB, et al. 1999. Mitogen-activated protein kinase (MAPK) regulates the expression of progelatinase B (MMP-9) in breast epithelial cells. Int J Cancer 82:268-73.

Sadakata S, et al. 1992. Mortality among female practitioners of Chanoyu (Japanese "tea-ceremony"). Tohoku J Exp Med 166:475-77.

Schecter A, et al. 1997. Dioxins, dibenzofurans, dioxin-like PCBs, and DDE in U.S. fast food, 1995. Chemosphere 34:1449-57.

Seo YR, et al. 2002. Selenomethionine induction of DNA repair response in human fibroblasts. Oncogene 21(23):3663-9.

Sharpe CR, et al. 2000. Nested case-control study of the effects of non-steroidal anti-inflammatory drugs on breast cancer risk and stage. Br J Cancer 83:112-20.
Shao Z, et al. 1998. Genistein exerts multiple suppressive effects on human breast carcinoma cells. Cancer Res 58:4851-57.

Slattery ML, et al. 2000. Carotenoids and colon cancer. Am J Clin Nutr 71:575-82.

Smith ML, et al. 2000. The effect of non-steroidal anti-inflammatory drugs on human colorectal cancer cells: evidence of different mechanisms of action. Eur J Cancer 36:664-74.

Smith WA, et al. 2001. Effect of chemopreventive agents on DNA adduction induced by the potent mammary carcinogen dibenzo[a]pyrene in the human breast cells MCF-7. Mutat Res 480:97-108.

Solomons NW. 1996. Plant sources of vitamin A and human nutrition: renewed strategies. Nutr Rev 54:89-91.

Song J, et al. Chemopreventive effects of dietary folate on intestinal polyps in Apc+/-Msh2-/-mice. Cancer Res 60:3191-9.

Voorrips LE, et al. 2000. A prospective cohort study on antioxidant and folate intake and male lung cancer risk. Cancer Epidem Biomarkers Prev 9:357-65.

Zhang S, et al. 1999. A prospective study of folate intake and the risk of breast cancer. JAMA 281:1632-7.

Zhang S, et al. 1999. Dietary carotenoids and vitamins A, C, and E and risk of breast cancer. J Natl Cancer Inst 91:547:56.

Zhou J, et al. 2002. Inhibition of orthotopic growth and metastasis of androgen-sensitive human prostate tumors in mice by bioactive soybean components. Prostate 53:743-53.


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