Researchers at Harvard report that various soy diets have significant effects against prostate cancer compared to a casein (milk protein) diet. The higher the amount, the greater the effect. Among other things, soy significantly reduced Insulin-like Growth Factor (IGF-1), a protein that helps tumors create blood vessels. Blood vessel density and tumor cell proliferation were decreased. Cell death was increased. The researchers concluded that dietary soy works through "a combination of direct effects on tumor cells and indirect effects on tumor neovasculature" (blood vessels) (Zhou et al. 1999). The cell-killing effects of soy products are important not only for men who have been diagnosed with prostate cancer, but for healthy men as well. Cancer cells can quietly multiply for years before they are discovered.

Prostate-specific antigen (PSA) is elevated in men with prostate enlargement. PSA is regulated by androgens. Anti-androgen drugs have undesirable side effects. An NIH study shows that genistein and its precursor, biochanin A, markedly decreased PSA in prostate cancer cells. It works by inactivating tes-tosterone (Sun et al. 1998). A study on rats shows a 38% decline in PSA, along with a huge reduction in metastases when genistein was given subcutaneously (Schleicher et al. 1999). Not only genistein, but 17 other plant compounds lower PSA in prostate (Zand et al. 2002).

Soy isoflavones work in cells, and they work in rodents. The big question is: Do they work in humans? Three new government-sponsored trials are taking place. One is on the ability of genistein to reduce cellular proliferation in men with elevated PSA. Another is on the ability of supplemental soy to lower PSA and kill cancer cells in men with localized prostate cancer. The third is on the ability of soy isoflavones to modulate hormones and cancer-related proteins in men with prostate cancer.

Although these are the first studies focused directly on using soy in humans to fight prostate cancer, population-based studies show that men with high levels of soy and other isoflavones in their blood have the lowest risk of prostate cancer. Some of these studies have looked at thousands of men. In a study on men from Japan, China, and the United States, it was shown that legumes, including soy, reduce the incidence of prostate cancer by 38%. Eating yellow-orange vegetables reduces it 33%, and cruciferous vegetables reduce it 39%. Findings are consistent across ethnicities, indicating that isoflavones, not genes, are responsible for the reductions in risk (Kolonel et al. 2000). These risk reduction numbers for soy are almost identical to those reported for rodents eating soy. An analysis of data collected from 12,395 Seventh-Day Adventist men indicates that more than one serving per day of soymilk can reduce the risk of prostate cancer 70% (Jacobsen et al. 1998). Note: Seventh-Day Adventists are vegetarians; meat is a known risk factor for prostate cancer. Being vegetarian may have contributed to the low rates.

Researchers at the University of Alabama have published a study showing that genistein down-regulates proteins that enhance prostate cancer growth, including that from HER2/neu. They conclude that genistein has no adverse toxicity--that the amount needed to reduce the proteins by half is achieved by supplemental genistein or a diet high in soy products. Their final words are the following: "Genistein inhibition of the EGF signaling pathway suggests that this phytoestrogen may be useful in both protecting against and treating prostate cancer" (Dalu et al. 1998).

Soy isoflavones clearly work against prostate cancer. They work through several mechanisms, including modulating hormones, blocking metastasis, interfering with cell signaling, stopping the growth of cells and killing them, and possibly activating and deactivating cancer-related genes.

Soy for Breast Cancer
Breast cancer is another hormone-related cancer that soy phytoestrogens help to prevent and control. It is especially beneficial for Western women, who are exposed to a comparatively high level of environmental estrogens. Soy is antiestrogenic. One way it works is to prevent the conversion of estrone to 17beta-estradiol, a "strong" estrogen. This is very important because estradiol fuels the growth of breast cancer, whereas estrone is a much weaker estrogen. Researchers who have investigated the effects of soy isoflavones on estrogen metabolism report that genistein causes cancer cells to metabolize estradiol to "estrogenically weaker or inactive metabolites" (Brueggemeier et al. 2001).

The big news on soy is the discovery of a new estrogen receptor that soy phytoestrogens naturally activate. The receptor, known as ERb, appears to suppress the activation of ERa, which allows growth-promoting estradiol into cancer cells (Pettersson et al. 2000). ERa is the receptor that everyone knows about and refers to when they say a cancer is "estrogen receptor positive." It turns out, however, that so-called "estrogen receptor negative" breast cancer cells actually have estrogen beta receptors. They simply were not detected until recently. Estrogen receptor positive cells have simply lost their beta receptors. It is believed that the loss of the beta receptor is one of the events leading to breast cancer. Normal cells have both types of receptors.

Genistein naturally activates ERb. When this receptor is activated, cell proliferation is inhibited. Researchers do not have the complete picture yet, but among other things, activating the beta receptor down-regulates the alpha, or estradiol-activated, receptor. This negates estradiol's cancer-promoting effects.

The results can be seen in humans. In a study from Vanderbilt University on Chinese women, the consumption of soy reduced the risk of having ERa positive breast cancer by 56%, whereas the effect on both types of breast cancer was about 30% (Dai et al. 2001).

Genistein also interferes with the cancer's ability to grow blood vessels. A direct link between alpha receptors and angiogenesis has been discovered in estrogen receptor positive cancer cells (MCF-7). These cells have too many alpha receptors and not enough beta. When estradiol gets into the alpha receptors, it activates a protein that promotes the formation of new blood vessels (Sampath et al. 2001). No experiment showing the direct effect of genistein on this protein has been done, but research shows that genistein blocks the formation of new blood vessels (Zhou et al. 1998; Wietrzyk et al. 2001).

It is interesting to note that vitamin D also suppresses the "bad" ERa. In one experiment on MCF-7 cells treated with the vitamin, there was a 50% reduction in the receptor at 24 hours (Stoica et al. 1999). Genistein keeps vitamin D from being degraded by cancer cells (Farhan et al. 2002).

In a study on estrogen receptor positive breast cancer cells (MCF-7), genistein competed successfully with estradiol for access to the cells, and once inside, blocked estradiol from making them grow. It is very likely that the low levels of estrogen in Asians and others is a result of their higher consumption of phytoestrogens, which block out stronger, growth-promoting estrogens. In a study on Japanese women who drank soymilk containing 100 mg of isoflavones a day, estrone and estradiol levels fell by almost 30% (Nagata et al. 1998).

Much research has been done on how cancer cells metabolize and utilize estrogen. Soy products have many different effects. For example, breast cancer cells have elevated levels of enzymes that produce estradiol. One of the enzymes is known as 17HSD1. 17HSD1 causes the conversion of "weak estrogen" (estrone) to "strong estrogen" (estradiol) and helps cancer cells grow. A variant known as 17HSD2 does the opposite. One of the abnormalities of breast cancer cells is that they have elevated amounts of 17HSD1, and insufficient 17HSD2 (Miyoshi et al. 2001). Studies show that if cancer cells are treated with genistein, more 17HSD2 will be made, and more "strong estrogen" (estradiol) will be converted to "weak" (estrone). Vitamin D does the same thing (Hughes et al. 1997). A woman with breast cancer may have the same level of estrogen in her blood as a woman without--the elevated estradiol levels are occurring inside cancer cells where abnormalities create imbalances in enzymes such 17HSD so as to favor the accumulation of estrogen for cell growth.

Genistein also inhibits an enzyme that is elevated in breast cancer cells known as "aromatase" (Kao et al. 1998; Breuggemeier et al. 2001). Aromatase helps convert testosterone to estrogen. Its importance in promoting hormone-related cancer is illustrated by an experiment on male mice that lack the enzyme. Elevated male hormones, enlarged prostate, and abnormal cell growth do not turn into prostate cancer in these mice that lack aromatase (McPherson et al. 2001).

Asian women are the best advertisement for the benefits of soy against breast cancer. They get early protection by eating soy their entire lives (Lamartiniere et al. 1998). The genistein in soy promotes more differentiated tissue in the breast, which leaves less that can turn cancerous. Soy isoflavones have the added benefit of making less dense areas in the breast so that cancer is easier to detect by mammogram (Maskarenic et al. 2001). A study from the University of Southern California shows that a serving of tofu every week decreases the risk of breast cancer by 15%. More tofu equals less risk (Wu et al. 1996). It is well established that when Asian women abandon their traditional diet, their risk of breast cancer escalates. It is important to realize, however, that while it is proven that soy products have direct and powerful effects against cancer cells, it cannot be assumed that soy alone is responsible for the reduced risk of hormone-related cancers in Asians. There are many other aspects of the Asian diet that undoubtedly play a role, including the low consumption of animal fat. Green tea is another component of the Asian diet that has proven anticancer effects. A study published in Cancer Letters shows that while a polyphenol from black tea has no effect on prostate cancer cells, when combined with genistein, it stops proliferation (Sakamoto 2000).

HER2/neu and EGFR are both related to breast cancers resistant to treatment with tamoxifen and other therapies (Ross et al. 1998). Therapy against this resistant cancer is currently a hot topic in research. Genistein blocks a chemical reaction that activates them by its ability to inhibit "protein L-Tyrosine kinases." Essentially what that means is that genistein blocks an enzyme that promotes the proliferation of cancer cells. Because protein L-Tyrosine kinases activate other cancer-promoting phenomena in other types of cancer, genistein is a very attractive candidate for the prevention and treatment of various types of cancer. In the one rodent study done on genistein, HER2/neu, and breast cancer, a dietary amount of the soy compound significantly delayed the appearance of the HER2/neu-type cancer. It did not, however, reduce tumor size or number in this study (Jin et al. 2002).

It is important to note that DDT and other chlorine-related chemicals activate protein L-Tyrosine kinases, including HER2/neu-related ones in human cancer cells. Although DDT was banned decades ago, it and its relatives are still being manufactured, and Americans are still being exposed to them. Genistein and other isoflavones block the activation of PTK by DDT and related estrogen-mimicking chemicals, but tamoxifen does not (Enan et al. 1998; Verma et al. 1998). Genistein was the most effective of the isoflavones tested in the Verma study.

The data on the benefits of soy against breast cancer are overwhelmingly positive, and more research needs to be done. Unfortunately, the word "phytoestrogen" has scared some people into thinking soy is estrogenic. Most phytoestrogens have no estrogenic activity whatsoever. Others have beneficial activity where it is needed, such as in bone and heart. That is why phytoestrogens have been characterized as "good" estrogen (Shao et al. 2000). For this reason, some researchers have reportedly objected to the term "phytoestrogen."

The anticancer effects of soy on breast cancer cells have been proven in dozens of studies. However, some researchers have reported that they can make the soy compound genistein act estrogenic in estrogen receptor positive cancer cells known as MCF-7 (Wang et al. 1997). The conditions that must be present for genistein to make this type of cell grow are highly abnormal. Only a minute amount of genistein can be added to the cells; any more and growth will be impeded, not promoted. In addition, there must be no other estrogen present, including environmental estrogen-mimicking chemicals (Verma et al. 1998). These conditions would not occur in humans.

However, one researcher has transferred this laboratory experiment to a mouse and reported that he can make genistein promote cancer growth (Helferich, see Santell et al. 2000). He is the only lead researcher who has been able to do this, and his research shows the exact opposite of all the cell culture studies showing that increasing amounts of genistein block cancer growth in a dose-dependent manner. His results also conflict with those of another researcher who has done a very similar mouse study showing that increasing amounts of genistein retard cancer growth, in accordance with the cell studies (Shao et al. 1998). One of the problems may be that the experiment is very difficult to do. The animals must be implanted with estradiol to make the cancer cells grow. There are many variables, including how the individual mice metabolize genistein. Unfortunately, even though the results of neither study have been confirmed, the negative findings have been published multiple times under different names, giving the illusion that the results have been independently confirmed (Santell et al. 2000; Allred et al. 2001; Ju et al. 2001). However, evidence to the contrary continues to accumulate. It has been reported that when mice are fed the equivalent of what Asians usually get in their diets, the appearance of a genetic type breast cancer (as opposed to a chemically induced one like the other studies) is significantly delayed by genistein, soy isoflavones, and daidzein, another soy compound (Jin et al. 2002).

The evidence for prostate cancer, another hormone-responsive cancer, is overwhelming. There is no question that the compounds from soy have multiple and powerful anticancer effects.

Studies in monkeys, the closest animal model to humans, show that soy phytoestrogens impede the proliferation of cells responsive to estrogen. Researchers who have been studying for decades the effects of different types of estrogens on monkeys state flatly: "Soybean phytoestrogens are not estrogenic at dietary doses" (Cline et al. 2001). Statistics on the rate of hormone-related cancers in Asians prove that soy is extremely beneficial against hormone-related cancers in humans. They show that people who eat large amounts of soy products have the lowest levels of strong estrogen in their bodies and the lowest rates of breast and prostate cancers. Numerous studies demonstrate the multiple effects soy has against cancer at the cellular level.

Soy and Other Types of Cancer
Soy has powerful anticancer effects that do not involve hormones. Although these other effects have not been as well researched, they are just as promising, especially for other types of cancer. Genistein has been the subject of most of the studies showing other effects. One of the effects is that this compound inhibits a chemical reaction used for many different types of cancer cells to multiply and spread. Compounds that can do this are called protein L-Tyrosine kinase (PTK) inhibitors. Dozens of studies in different types of cells show that genistein is a powerful and effective PTK inhibitor.

Glioma.
Glioma cancer cells have very high PTK activity. That activity correlates with cancer growth. Several in vitro studies show that genistein inhibits the growth of glioma (Baltuch et al. 1996; Tu et al. 2000; Khoshyomn et al. 2002). Genistein also enhances the effectiveness of the chemotherapeutic drugs carmustine and camptothecin with a 40% decrease in growth and a 50% increased killing effect in some cells, according to one study (Ciesielski et al. 1999; Khoshyomn et al. 2002). The amount needed to enhance the effectiveness of carmustine is not extremely high. The appropriate amount of genistein can be obtained by following the supplement program recommended in the Soy Dosing and Precautions section.

Bladder Cancer.
Genistein's ability to inhibit PTK may be of great benefit in keeping bladder cancer localized. In Asia, the incidence of invasive bladder cancer is much lower than in the United States, leading some researchers to investigate the effects of soy. Researchers at the University of Virginia have shown that invasive bladder cancers have high levels of a protein known as epidermal growth factor receptor (EGFR), which enables the cancer to invade muscle. This is the event that causes bladder cancer to go from something treatable to something very dangerous. EGFR is activated by PTK and can be reversed by genistein. This and other research shows that drugs designed to inhibit PTK do not work any better than genistein (Theodorescu et al. 1998).

The effects of genistein, soy protein isolate, and soy phytochemical concentrate on human bladder cancer cells and bladder cancer in mice were studied by researchers at Harvard. The three soy products reduced tumor volume 40%, 37%, and 48%, respectively. They blocked blood vessel formation and induced cell death, stopping the cells from growing at the GM-2 part of the cell cycle (Zhou et al. 1998).

Chinese researchers report that a mixture of isoflavones works better than a single soy compound for bladder cancer. In their study on seven different cell lines, genistein plus isoflavones inhibited tumor growth and induced cell death at levels obtainable through the diet or supplements. After studies on mice, they concluded that "both genistein and combined isoflavones exhibited a significant tumor suppressor effect in vivo. The results justify the potential use of soybean foods as a practical chemoprevention approach for patients with urinary tract cancer" (Su et al. 2000).

Stomach Cancer
Japanese researchers tested the effects of soy products on 10 different types of human gastrointestinal cancer cells. They found that genistein and biochanin A (a precursor) strongly inhibited proliferation of stomach, colon, and esophageal cancers (Yanagihara et al. 1993). Other researchers in Japan analyzed data from a study involving over 30,000 people and found that people who eat the most soy products reduced their risk of stomach cancer by half compared to those who eat the least (Nagata et al. 1998).

Melanoma
Melanoma is one of the least treatable cancers. Anything that could help stop this type of cancer cell would be welcome. Researchers in France are studying the effects of genistein on human melanoma cancer cells. They report that genistein is a powerful inhibitor of the growth of this cancer and that it stops the cell cycle as well as the chemotherapeutic drugs adriamycin and etoposide. Caffeine reverses the beneficial effects (Darbon et al. 2000).

Polish researchers studying melanoma in mice have shown that genistein reduces the blood supply to lung tumors and has an additive effect with the drug cyclophosphamide. In laboratory rodents, genistein can reduce the growth of tumors by half if given before and after cancer. The amount needed can be obtained through supplements and/or diet (Record et al. 1997).

Lung Cancer
Research on lung cancer cells and tumors shows that genistein has several actions against small cell and nonsmall cell lung cancer. In a study in which Lewis lung cancer was transplanted into mice, genistein reduced the tumor colonies by half, and genistein plus cyclophosphamide reduced them 90% (Wietrzyk et al. 2001). Several studies show that genistein stops lung cancer cells from growing and then induces cell death (Tallett et al. 1996; Fujimoto et al. 2002; Wietrzyk et al. 2000). Genistein also inhibits enzymes that help lung cancer cells to proliferate and spread (Leyton et al. 2001). Researchers at Wayne State have also demonstrated that genistein upregulates tumor suppressor genes p53 and p21 (Lian et al. 1999). Other research shows that genistein reverses the multidrug resistance-associated protein, a protein that makes lung cancer cells resistant to daunorubicin, doxorubicin, etoposide, and vinblastine (Versantvoort et al. 1994; Berger et al. 1997).

Researchers in Japan analyzed information from 333 people with lung cancer. They found that eating tofu every day reduced the risk of lung cancer 45% in men and 86% in women (Wakai et al. 1999).

Colon Cancer
Soy has anticancer effects against the type of cells that line the digestive tract. For this reason, it may have good effects against different types of digestive tract cancers. Researchers looking at how three different types of human colon cancer cells react to soy confirm that this type of cancer is susceptible to soy's anticancer effects (Zhu et al. 2002). Some colon cancers are estrogen dependent. Researchers in Italy have shown that estradiol activates four kinase enzymes in colon cancer cells, two of which are L-Tyrosine dependent and therefore potentially susceptible to genistein. Researchers were able to show that genistein blocks at least one of them and retards cell growth (Di Domenico et al. 1996). Genistein also suppresses the growth of nonestrogen-dependent colon cancer cells, which also respond to treatment with tamoxifen (Arai et al. 2000). In a study that looked at how tamoxifen, genistein, and estradiol affect intestinal cells, genistein and tamoxifen emerged as the strongest inhibitors of cell proliferation. They both inhibit PTK and induce the death of cancer cells (Booth et al. 1999). Researchers in the United States have reported that genistein reverses resistance to doxorubicin and other chemotherapeutic drugs in at least one type of colon cancer by a "novel drug resistance pathway" (Rabindran et al. 1995). However, a study in mice shows that soy isoflavones may not save you from a bad diet. Mice fed a Western high fat, low fiber, and low calcium diet developed colon cancer despite getting isoflavones in their food (Sorensen et al. 1998). And another study on mice getting high fat diets also found that soy could not reverse colon cancer (but rye lignans could) (Davies et al. 1999).

Thyroid Cancer.
Soy may have beneficial effects against other types of cancer, including thyroid cancer. Researchers at the Northern California Cancer Center looked at 608 cases of thyroid cancer, a relatively large number of cases. They found that people who got soy compounds, genistein and daidzein, in their diet reduced their risk of this cancer by one-third. (Alfalfa sprouts reduced risk by almost half (Horn-Ross et al. 2002). However, adding soy flour or protein to a Western diet was not effective.

Leukemia.
A few studies have been done on human leukemia cells treated with genistein. In a report from Japan, genistein showed the strongest antigrowth effects against HL-60 cells of nine compounds tested. All nine compounds are found in miso (Hirota et al. 2000). In another study on the same type of cells that were made resistant to chemotherapy, genistein was able to reverse the drug resistance almost completely (Nagasawa et al. 1996). In a third study, the antiproliferative effect of genistein against human leukemia was significantly augmented by vitamin D analogs (Siwinska et al. 2001).

Free-Radical Scavenging Effects
With all of the new information on the exotic ways soy compounds can prevent and suppress cancer, it is easy to forget one of its most important benefits. The antioxidant effects of soy were the focus of much of the early research on how it prevents cancer. Studies are still being published on the powerful antioxidant, free-radical scavenging effects of soy compounds and how they impact cancer.

Soy has an additive effect with vitamin E and lowers rather than elevates estrogen levels in women and androgen levels in men (Jenkins et al. 2000). Damage to DNA caused by certain types of free radicals is strongly inhibited by genistein and other soy compounds (Breinholt et al. 1999; Davis et al. 2001). This helps prevent cancer, and it does not take extraordinary amounts to get powerful antioxidant effects. Dietary amounts significantly lower free-radical damage (Davis et al. 2001; Exner 2001).

In addition to blocking free-radical damage, soy phytoestrogens also block inflammation, a newly discovered contributor to cancer growth, notably in the colon (Davis et al. 2001; Zheng et al. 2002).

The effects of genistein against the activation of EGFR by free radicals were demonstrated in a study from Boston University. In this study, genistein reversed the free-radical activation of EGFR in normal cells (Chen et al. 2001). The benefits and uniqueness of genistein against oxidative stress are evident in a study on brain cells exposed to hydrogen peroxide. For the first time researchers in Spain recently demonstrated that free radicals generated by this oxidant degrade phospholipids, which are crucial for memory and other aspects of brain function. The breakdown occurs because the radicals activate enzymes. Genistein comes to the rescue again through its ability to inhibit a protein kinase enzyme that sets off the reaction (Servitja et al. 2000). The ability of soy to block free radicals not only helps prevent cancer from occurring in the first place, but it also helps block it if it does occur.

Soy Precautions and Dosage
While the data are persuasive regarding the chemoprotective effects of soy, many questions remain. Some nutritionally based oncologists do not permit soy in their patients' regime. Others believe that soy should be avoided by everyone and have launched massive public relations campaigns to discredit soy and discourage even moderate consumption by healthy people.

Estrogen-receptor positive breast cancer patients should avoid genistein until the exact type of estrogen receptor has been identified. Alpha-estrogen receptor positive breast cancers may benefit from genistein, while beta-receptor positive breast cancers cells may proliferate faster in response to genistein. It has been suggested that patients avoid soy supplements 1 week prior to, during, and 1 week after radiation therapy, although new studies appearing in the Cancer Radiation Therapy protocol indicate a potential benefit to using soy isoflavones during radiation therapy.

Some people believe that soy is toxic to the thyroid gland, yet this may be a concern only in cases of iodine deficiency. Some of the more credible attacks deal with soy-based infant formulas.

There are a number of human clinical studies being conducted on the use of soy to both prevent and treat cancer. When the findings of these studies are published, perhaps more definitive recommendations can be made about soy. Based on the information available to us as of this writing, those concerned about cancer may consider these guidelines: a suggested therapeutic soy extract dosage is five 700-mg capsules 4 times a day of a soy extract providing a minimum of 40% isoflavones. For prevention purposes, as little as 135 mg of a 40% soy isoflavone extract once a day may be adequate.

Theanine--increases efficacy of chemotherapeutic drugs
Researchers speculate that drinking 1 cup of green tea favors a positive mental attitude and increases the efficacy of the chemotherapeutic index. But, components of green tea have been identified (caffeine, epigallocatechin gallate (EGCG), flavonoids, and theanine) that better explain the chemotherapeutic advantage beyond its soul-soothing effects (Sadzuka et al. 2000a).

Japanese researchers focused specifically on thea-nine and its influence on the antitumor activity of Adriamycin (doxorubicin). In vitro, theanine inhibited the outflow of Adriamycin (ADR) from cancerous cells, increasing concentrations within the cell by almost threefold. An increase in ADR concentrations was not observed in normal tissues, suggesting thea-nine protects vulnerable organs, such as the heart and liver, from chemical poisoning (Sadzuka et al. 1996). Illustrative of the enhancing qualities of theanine, injecting ADR into M5076 ovarian sarcoma-bearing mice did not inhibit tumor growth, whereas a combination of theanine and ADR reduced tumor weight 62% (Sugiyama et al. 1998).

When theanine was added to pirarubicin, intracellular concentrations of pirarubicin increased 1.3-fold and the overall therapeutic efficacy of the drug increased 1.7-fold (Sugiyama et al. 1999). Gratifying results also occurred when theanine was used with Idarubicin (IDA), which is highly toxic to bone marrow and an antileukemia agent similar to doxorubicin. Because of risk factors, only about one-fourth of the standard IDA dose was used in combination with theanine. However, theanine reduced toxicities and increased IDA antitumor activity, rendering the chemotherapeutic agent a possibility for the treatment of leukemia (Sadzuka et al. 2000b).

Part of theanine's amazing performance can be attributed to mimicking glutamate, an amino acid that potentiates glutathione. Cancer uses glutathione to detoxify chemotherapeutic agents, barricading chemicals from cells, and inhibiting a kill. Theanine's structural similarity is the key, crowding out glutamate transport into tumor cells. Cancer cells (in confusion) erringly take in theanine and theanine-created glutathione results. Glutathione (created by theanine) does not detoxify like natural glutathione, and instead it blocks the ability of cancer cells to neutralize cancer-killing agents. Deprived of glutathione, cancer cells cannot evict chemotherapeutic agents, and the cell dies as a result of chemical poisoning (Sadzuka et al. 2001).

Administered in union with doxorubicin, the suggested dose of theanine is 500-1000 mg a day, although no human studies have been conducted.

Thymus Extract--improves T-cell response and regulates the activity of cytokines
The thymus gland was at one time carelessly removed as an unnecessary appendage. It is in fact an essential organ of the immune system, increasing stamina, energy, well-being, and the ability to ward off infections and cancer. Since 1965, when Burnet was awarded the Nobel Prize for demonstrating the endocrine function of the thymus gland, medical interest has focused on the thymus. It is now largely accepted that the thymus gland plays a central role in the mammalian immune system.

One of two different divisions of the immune system is made up of B-cells that protect against bacterial and viral infections and T-cells that guard against viral and fungal infections, as well as cancer. This powerful body of cells normally treats a developing cancer as foreign tissue, destroying aberrant cells before rapid multiplication occurs.

The worthiness of T-cell mediated immunity depends upon the activity of T-lymphocytes (T-cells), which are programmed by proteins from the thymus gland. T-4 cells are immature (naïve) in the beginning, that is, they do not function properly until programmed by thymic proteins. T-cell education begins as new T-lymphocytes migrate from the bone marrow to the thymus, where they are programmed to distinguish between self-tissue (the host) and nonself tissue (an invading pathogen).

The thymus gland, a lymphoid organ situated in the anterior superior mediastinum, reaches its maximum weight near puberty and then undergoes involution, or degenerative change, shrinking to about one-sixth of its original size. By the age of 40, the thymus gland is scarcely functional in many individuals; therefore, the essential thymus-provided protein is no longer available to program T-4 cells. The dilemma is amendable because more than 20 years ago, Dr. Terry Beardsley, an immunologist, discovered thymic protein A, an isolated and purified protein derived from bovine thymus cells. Dr. Beardsley patented a technology to grow thymus cells in the laboratory and then purify a specific thymus protein (Thymic Protein A) that helps T-cells to mature with immune competency. The active ingredient in Thymic Protein A is the precise thymus protein that programs the T-4 lymphocytes to locate abnormal cells and then directs T-8 killer cells to destroy them.

The three different types of cells emerge from the thymus: T-4 helper cells (master regulators), T-8 cytotoxic killer cells (guided by T-4 helper cells to attack and destroy invading cells), and T-8 suppressor cells (necessary to terminate the attack once the battle is won). Of all the cells in the immune system, T-4 helper cells hold major rank because they regulate many key functions, including the activity of IL-2 and interferon. Scientists agree that abnormal cells, such as cancer or tumor cells, develop in the body every day; however, not everyone is diagnosed with cancer. The 24 who do not fall ill have a strong immune response (T-cell-mediated immunity) that effectively destroys aberrant cells.

Dr. Paul Chretien (National Cancer Institute, Bethesda, MD), administered high dose thymosin, a humoral factor secreted by the thymus, in conjunction with intensive chemotherapy to 21 patients with advanced lung cancer. Ordinarily, patients with late stage lung cancer live about 240 days; the median survival rate more than doubled (500 days) among patients receiving thymosin. Some of the thymosin-treated group were alive and disease-free 2 years later (Chretien et al. 1979).

Blood tests to measure the immune response are extremely valuable when detailing either a preventive or a therapeutic program to fight cancer. While determining T-lymphocyte numbers is important, assessing their activity is even more crucial. It is possible for a person with a total count of 1000 T-4 cells to have only 50% of these cells activated by the thymus. It is important that the patient know the degree of immune impairment in order to structure a corrective program. Tests to evaluate the activity of the immune system are performed at the Immuno-Science Laboratory (Los Angeles), (310) 657-1077.

A suggested dosage for healthy individuals is 1 packet of BioPro Thymic Protein A daily or every other day. Cancer patients may wish to increase this amount. For example, HIV patients use 3 doses a day until blood tests remain normal for 3-6 months. For maintenance, reduce to 1 dose a day. Use the thymic protein sublingually, retaining for 3 minutes to allow for maximum absorption. Typically, patients undergoing chemotherapy maintain acceptable white blood cell counts if Thymic Protein A accompanies treatment.

Vitamin A--offers protection against radiation induced tissue damage, downregulates telomerase activity, and is involved at almost every juncture of cancer control
In 2001, a study released from the Kyushu University Graduate School of Medical Science confirmed that retinoids induce cell differentiation, control cancer growth and angiogenesis, repair precancerous lesions, prevent secondary carcinogenesis and metastasis, and act as an immunostimulant. The Kyushu researchers also noted that after FAR therapy (5-fluorouracil-retinil palmitate with radiation and surgery), the disease-specific, 5-year survival was nearly 50% in various head and neck cancers (Yamamoto 2001). Favorable odds were bolstered as retinoids, at pharmacological levels, assist in preventing the appearance of secondary tumors following curative therapy for epithelial malignancies.

It is well established that a vitamin A deficiency (in laboratory animals) correlates with a higher incidence of cancer and an increased susceptibility to chemical carcinogens. This is in agreement with epidemiological studies, indicating individuals with a lower dietary vitamin A intake are at a higher risk of developing cancer (Sun et al. 2002). Considering statistics, the chemotherapeutic possibilities surrounding vitamin A are manifold.

Cancer Adjuvant Therapy Pg (1) (2) (3) (4) (5) (6) (7)

These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease