Natural Therapies
In 1991, researchers at the Institute for Hormone Research announced that they had been able to induce the body to convert the stronger form of estrogen (estradiol) into the weaker form (estriol) without using drugs. Estriol is considered to be a more desirable form of estrogen. It is less active than estradiol, so when it occupies the estrogen receptor, it blocks estradiol's strong "grow" signals. It took only 1 week to prove that the conversion of estradiol to estriol could be accomplished without drugs. Using a natural substance, researchers were able to increase the conversion of estradiol to estriol by 50% in 12 healthy people (Michnovicz et al. 1991). Next, they tested the natural substance in female mice prone to developing breast cancer. The incidence of cancer and the number of tumors fell significantly. The substance was indole-3-carbinol (IC3), a phytochemical isolated from cruciferous vegetables (broccoli, cauliflower, Brussels sprouts, turnips, kale, green cabbage, mustard seed, etc.). I3C was then given to 17 men and women for 2 months. Again, levels of strong estrogen declined, and levels of weak estrogen increased. But more importantly, the level of an estrogen metabolite associated with breast and endometrial cancer (16,alpha-hydroxyestrone) fell (Bradlow et al. 1991). In 1997, researchers at Strang Cancer Research Laboratory at Rockefeller University discovered that when I3C changes "strong" estrogen to "weak" estrogen, the growth of human cancer cells is inhibited by 54-61% (Telang et al. 1997). More important to breast cancer patients, this study demonstrated that I3C provoked cancer cells to self-destruct (apoptosis). A prime goal of cytotoxic chemotherapy is to induce apoptosis. If future studies show that nontoxic I3C can reliably facilitate apoptosis, this phytonutrient may become a standard adjunct in the treatment of breast cancer. Subsequent studies done at the University of California at Berkeley show that I3C inhibits MCF7 human breast cancer cells from growing by as much as 90% in culture. Growth arrest does not depend on estrogen receptors (Cover et al. 1998). I3C does more than just turn strong estrogen to weak estrogen. 16,alpha-hydroxyestrone (16OHE) and 2-hydroxyestrone (2OHE) are metabolites of estrogen in addition to estriol and estradiol. 2OHE is biologically inactive, while 16OHE is biologically active; that is, like estradiol, it can send "grow" signals. In breast cancer, the dangerous 16OHE is often elevated, while the protective 2OHE is decreased. Interestingly, cancer-causing chemicals change the metabolism of estrogen so that 16OHE is elevated. Studies show that people who take I3C not only have beneficial increases in the "weak" estriol form of estrogen, but they also have increases in protective 2OHE. In an experiment at New York University, researchers gave African-American women I3C, 400 mg for 5 days. Most of them experienced an increase in the "good" 2OHE and a decrease of the "bad" 16OHE. However, some did not. It was found that those who did not, had a mutation in a gene that helps metabolize estrogen to the 2OHE version. These women have an eight times higher risk of breast cancer (Telang et al. 1997). I3C Stops Cancer Cells from Growing Tamoxifen is a drug prescribed to reduce metastatic risk and improve survival. I3C has modes of action similar to tamoxifen. In studies from the University of California mentioned above, I3C inhibited the growth of estrogen-receptor-positive breast cancer cells by 90% compared to 60% for tamoxifen. The mode of action attributed to I3C's impressive effect was interfering with the cancer cell growth cycle. Adding tamoxifen to I3C gave a 5% boost (95% total inhibition) (Cover et al. 1999). In estrogen-receptor-negative cells, I3C stopped the synthesis of DNA for new cells by about 50%, whereas tamoxifen had no significant effect. I3C also restored p21 and other proteins that act as checkpoints during the synthesis of a new cell. Tamoxifen showed no effect on p21. Restoration of these growth regulators is extremely important. For example, tumor suppressor p53 works through the p21 that I3C restores. I3C also inhibits cancers caused by other types of chemicals. If animals are fed I3C before exposure to cancer-causing chemicals, DNA damage and cancer are virtually eliminated (Guillot et al. 1996). A study on rodents shows that damaged DNA in breast cells is reduced 91% by I3C. Similar results are seen in the liver (Devanaboyina et al. 1997). And in a study from New York University Medical Center, female smokers taking 400 mg of I3C significantly reduced their levels of a major lung carcinogen. Cigarette chemicals are known to adversely affect estrogen metabolism (Taioli et al. 1997). There is no proven way to prevent breast cancer, but the best and most comprehensive scientific evidence so far supports phytochemicals such as I3C. I3C beat out more than 80 other substances, including tamoxifen, for anticancer potential in one assay. Researchers at the Hoechst Marrion Roussel drug company staked their claim to dozens of indole-3 look-alikes. They claim that the indoles, which down-regulate estrogen receptors, can be used to treat and prevent cancer and autoimmune diseases such as multiple sclerosis, arthritis, and lupus. They hope to replace all the chemically altered estrogen drugs, such as tamoxifen, with a new generation of chemically altered indole drugs that fit in the Ah receptor and regulate estrogen indirectly (Bitonti et al. 1999). A summary of recent studies shows that indole-3-carbinol (I3C) can:
While the evidence is compelling, it is too soon to know exactly how effective I3C will be as an adjuvant breast cancer therapy (see the Breast Cancer References for citations pertaining specifically to I3C). Suggested dosage: Take one 200-mg capsule of I3C twice a day, for those under 120 pounds. For those who weigh more than 120 pounds, three 200-mg capsules a day may be needed. Women who weigh over 180 pounds should take four 200-mg I3C capsules a day. Note: A little is good; a lot is not necessarily better. Too much I3C can have the opposite effect of what you want. Therefore, do not exceed the dosage. Caution: Pregnant women should not take I3C because of its modulation of estrogen. The reported aversion to cruciferous vegetables by pregnant women may be associated with their ability to change estrogen metabolism. Estrogen is a growth factor for the fetus. Curcumin Curcumin is extracted from the spice turmeric and is responsible for the orange/yellow pigment that gives the spice its unique color. Turmeric is a perennial herb of the ginger family and a major component of curry powder. It has been safely used for centuries by Chinese and Indian people, both in herbal medicine and in food preparation. Curcumin has a number of biological effects in the body. However, one of the most important functions is curcumin's ability to inhibit growth signals emitted by tumor cells that elicit angiogenesis (growth and development of new blood vessels into the tumor). Curcumin inhibits the epidermal growth factor receptor and is up to 90% effective in a dose-dependent manner. It is important to note that while curcumin has been shown to be up to 90% effective in inhibiting the expression of the epidermal growth factor receptor on cancer cell membranes, this does not mean it will be effective in 90% of cancer patients or reduce tumor volume by 90%. However, because two-thirds of all cancers overexpress the epidermal growth factor receptor and such overexpression frequently fuels the metastatic spread of the cancer throughout the body, suppression of this receptor is desirable. Other mechanisms of curcumin include:
Curcumin's effects are a dose dependent response, and a standardized product is essential. The recommended dose is four 900-mg capsules 3 times per day, preferably with food. Green Tea As a tumor grows, it elicits new capillary growth (angiogenesis) from the surrounding normal tissues and diverts blood supply and nutrients away from the tissue to feed itself. Unregulated angiogenesis can facilitate the growth of cancer throughout the body. Antiangiogenesis agents inhibit this new capillary growth, and green tea is one of these agents. Green tea contains epigallocatechin gallate EGCG, a polyphenol that helps to block the induction of vascular endothelial growth factor (VEGF). Scientists consider VEGF essential in the development of angiogenesis and endothelial cell survival. It is the EGCG fraction of green tea that makes it a potentially effective adjunct therapy in the treatment of breast cancer. In vivo studies have shown green tea extracts to have the following actions on human cancer cells (Jung et al. 2001b):
However, there are benefits to obtaining some caffeine. Studies show that caffeine potentiates the anticancer effects of tea polyphenols, including the critical EGCG. Caffeine will be discussed in further detail later in this protocol. (Green tea extract is available in a decaffeinated form for those sensitive to caffeine or those who want to take the less-stimulating decaffeinated green tea extract capsules for their evening dose.) Conjugated Linoleic Acid (CLA) Conjugated linoleic acid (CLA) is a component of beef and milk and is essential for the transport of dietary fat into cells, where it is used to build muscle and produce energy. In a study in rats reported in the July 1999 issue of Experimental Cell Research , CLA was shown to prevent mammary cancer if given before the onset of puberty. And even more important, if CLA was ingested during the time of the "promotion" phase of cancer development, the rats were conferred substantial protection from further developing breast cancer. Another significant finding was that CLA appeared to actually inhibit the growth of normal mammary epithelial cell organoids and induced apoptosis (or cell death) in those same cells. The researchers concluded that this led to a reduction in the density of the developing mammary glands in rats, and, therefore, the incidence of breast cancer was reduced (Ip et al. 1999b). CLA may work via a mechanism similar to that of antidiabetic drugs such as Avandia and Actos by not only enhancing insulin-sensitivity but also protecting against cancer. A report in the September 2000 issue of the journal Medical Hypotheses pointed out that a number of human cancer cell lines express the PPARgamma transcription factor, and agonists for PPARgamma can promote apoptosis in these cell lines and impede their clonal expansion both in vitro and in vivo. CLA can activate PPARgamma in rat adipocytes, possibly explaining CLA's antidiabetic effects in Zucker fatty rats. The report concluded by stating: "It is thus reasonable to suspect that a portion of CLA's broad spectrum anticarcinogenic activity is mediated by PPARgamma activation in susceptible tumor" (McCarty 2000). Note: The term PPARgamma is an acronym for peroxisome proliferator activator-receptors-gamma. A PPAR gamma agonist such as Avandia, Actos, or CLA activates the PPARgamma receptor. This class of drug is being investigated as a potential adjuvant therapy against certain types of cancer.) Another finding that provides insight into the biochemical action of CLA is its ability to suppress arachidonic acid. Since arachidonic acid can produce inflammatory compounds that can aid cancer proliferation, this may be yet another explanation for CLA's anticancer effects. A study in the Journal of Nutrition demonstrated significant cancer-preventing properties when CLA was added to the diet. The study revealed CLA to be a "potent cancer preventative agent in animal models." Specifically, it was determined that feeding CLA to female rats while they were young and still developing conferred life-long protection against breast cancer. This preventative action was achieved by adding only enough CLA to equal 0.8% of the animal's total diet (Ip et al. 1999a). This compares favorably with Life Extension's recommendation of 3000-4000 mg daily, which is approximately 1% of the average human diet. The suggested amount required to obtain the overall cancer-preventing effects is only 3000-4000 mg daily in divided doses. Note: A combination product called Super CLA with Guarana may be used instead of CLA alone. Guarana is an herb that contains a form of caffeine called guaranine, which is 2.5 times stronger than the caffeine found in coffee, tea, and soft drinks. What makes guaranine unique from caffeine found in beverages is its slower release. That's because the guarana seed is fatty (even in powder form) and is not readily water-soluble. As mentioned earlier in this protocol and discussed subsequently, caffeine has an inhibitory effect on the growth of cancer and is synergetic with other natural compounds. Caffeine Caffeine occurs naturally in green tea and has been shown to potentiate the anticancer effects of tea polyphenols. The Journal of Nutrition and Cancer reported a study in which SKH-1 mice, which were at high risk of developing malignant and nonmalignant tumors, received oral caffeine as their sole source of drinking fluid for 18-23 weeks to ascertain the inhibitory effects of caffeine. The study revealed that caffeine inhibited the formation and decreased the size of both nonmalignant tumors and malignant tumors (Lou et al. 1999). In cancer cells, p53 gene mutations are the most common alterations observed (50-60%) and are a factor in both carcinomas and sarcomas. Caffeine has been shown to potentiate the destruction of p53-defective cells by inhibiting the gene's growth signal (G2). The effects of this are to inhibit and override the DNA damage-checkpoint and thus kill dividing cells. This capability of caffeine is important because the basis of many anticancer therapies is the use of genotoxic agents that damage DNA and destroy the replicating cells. Caffeine uncouples cell-cycle progression by interfering with the replication and repair of DNA. Caffeine therefore serves as a model compound, establishing the principle that agents that override DNA- damage-checkpoints can be used to sensitize cells to the killing effects of genotoxic drugs. This effect has been demonstrated by several independent research studies and reported in a number of primary journals (Sakurai et al. 1999a,b; Jiang et al. 2000; Valenzuela et al. 2000). Melatonin One of the most important supplements for a breast cancer patient is the hormone melatonin. High doses of the hormone should be taken at bedtime. Melatonin blocks estrogen receptors somewhat similarly to the drug tamoxifen without that drug's long-term side effects. Furthermore, when melatonin and tamoxifen are combined, synergistic benefits occur. Melatonin can be safely taken for an indefinite period of time. The suggested dose of melatonin for breast cancer patients is 3-50 mg at bedtime. Melatonin not only blocks estrogen-receptor sites on breast cancer cells, but directly inhibits breast cancer cell proliferation and boosts the production of immune components that kill metastasized cancer cells. There have been some studies demonstrating changes in melatonin and other hormone levels in breast cancer patients; specifically, women with breast cancer were found to have lower melatonin levels than women without breast cancer (Oosthuizen et al. 1989). Normally, women undergo a seasonal variation in the production of certain hormones, such as melatonin. The women with breast cancer did not have a seasonal variation in melatonin levels, as did the healthy women (Holdaway et al. 1997). Of course, this raises the question: Are these findings a contribution to the cause of breast cancer or a result of the disease? Se-Methylselenocysteine A new and better form of selenium is Se-methylselenocysteine, a naturally occurring organic selenium compound found to be an effective chemopreventive agent. SeMSC is a selenoamino acid that is synthesized by plants such as garlic and broccoli. Methylselenocysteine (MSC) has been shown to be effective against mammary cell growth both in vivo and in vitro (Sinha et al. 1999) and has significant anticarcinogenic activity against mammary tumorigenesis (Sinha et al. 1997). Moreover, a recent study has demonstrated that Se-methylselenocysteine was one of the most effective selenium compounds at chemoprevention and induced apoptosis in HL-60 leukemia cells (Jung et al. 2001a). Some of the most impressive data suggest that exposure to MSC blocks clonal expansion of premalignant lesions at an early stage. This is achieved by simultaneously modulating certain molecular pathways that are responsible for inhibiting cell proliferation and enhancing apoptosis (Ip et al. 2000a). Se-methylselenocysteine has been shown to:
Unlike SMC, which is incorporated into protein in place of methionine, SeSMC is not incorporated into any protein, thereby offering a completely bioavailable compound. In animal studies, SeSMC has been shown to be 10 times less toxic than any other known form of selenium. Breast cancer patients may consider taking 400 mcg of SeSMC a day. CoQ10 Since the 1960s, studies have shown that cancer patients often have decreased blood levels of coenzyme Q10 (Lockwood et al. 1995; Folkers 1996; Ren et al. 1997; Portakal et al. 2000; NCCAM 2000). These findings sparked interest in the compound as a potential anticancer agent (National Center for Complementary and Alternative Medicine 2001). Cellular and animal studies have found evidence that CoQ10 stimulates the immune system and can increase resistance to illness (Bliznakov et al. 1970; Hogenauer et al. 1981; NCCAM 2000). CoQ10 has demonstrated promise in treating breast cancer. Although there are only a few studies, the safe nature of CoQ10 coupled with this promising research suggests that breast cancer patients should take 100 mg 3 times a day. It is important to take CoQ10 with some kind of oil, such as fish or flax, because dry powder CoQ10 is not readily absorbed without it. There are more promising results for the use of CoQ10 to protect against heart damage related to chemotherapy. Many chemotherapy drugs can cause damage to the heart (UTH 1998; ACS 2000; NCCAM 2000; Dog et al. 2001), and initial animal studies found that CoQ10 could reduce the adverse cardiac effects of these drugs (Combs et al. 1977; Choe et al. 1979; Lubawy et al. 1980; Usui et al. 1982; Shinozawa et al. 1993; Folkers 1996). Some studies indicate that CoQ10 should not be taken at the same time as chemotherapy. If this is true, it would be disappointing, because CoQ10 is so effective in protecting against adriamycin-induced cardiomyopathy. Adriamycin is a chemotherapy drug sometimes used as part of a chemotherapy cocktail. Until more research is known, it is not possible to make a definitive recommendation concerning taking CoQ10 during chemotherapy. For more information please see the Cancer Chemotherapy protocol. EPA and DHA Omega-3 fatty acids, primarily EPA and DHA found in fish oil, have been shown to inhibit tumor development and metastasis. Further studies have demonstrated antiproliferative effects with increased lipid peroxidation. With large doses of fish oil, omega-3 fatty acids can inhibit cell proliferation and tumor growth through a free radical-mediated mechanism, while at more moderate doses, omega-3 fatty acids inhibit inflammation, angiogenesis, ras protein activity, or invasion enzymes. The recommended dosage is to consume a fish-oil concentrate supplement that provides 3200 mg of EPA and 2400 mg of DHA a day. This can be taken in divided doses. Vitamins A, D, and E Vitamin A and vitamin D3 inhibit breast cancer cell division and can induce cancer cells to differentiate into mature, noncancerous cells. Vitamin D3 works synergistically with tamoxifen (and melatonin) to inhibit breast cancer cell proliferation. Breast cancer patients should take 4000-6000 IU of vitamin D3 every day on an empty stomach. Water-soluble vitamin A can be taken in doses of 100,000-300,000 IU every day. Monthly blood tests are needed to make sure toxicity does not occur in response to these relatively high daily doses of vitamin A and vitamin D3. After 4-6 months, the doses of vitamin D3 and vitamin A can be reduced. Vitamin E succinate has been shown to inhibit tumor cell growth in vitro and in vivo. In a recently published study, vitamin E succinate, a derivative of fat-soluble vitamin E, inhibited growth and induced apoptic cell death in estrogen receptor-negative human breast cancer cell lines. The study concluded that vitamin E succinate might be of clinical use in the treatment of aggressive human breast cancers, particularly those that are resistant to antiestrogen therapy. Those with estrogen-receptor-negative breast cancers should consider taking 1200 IU of vitamin E succinate a day. When taking doses of vitamin D3 in excess of 1400 IU a day, regular blood chemistry tests should be taken to monitor kidney function and serum calcium metabolism. Continued . . . |
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