More than 4 million Americans are currently being treated for cancer. Each year, 1.3 million Americans are newly diagnosed with cancer. For the past four decades, both the incidence and age-adjusted death rate from cancer in America have been climbing steadily.

Cancer is an abnormal growth, caused by underlying disease involving the whole body. It is not just limited to a lump or bump. The successful treatment of cancer is best accomplished by the precise administration of multiple therapies. Neither conventional nor alternative medicine recognizes the importance of multimodality treatment, and the end result is that too many cancer patients needlessly die.

Although the mainstream therapies of chemotherapy, radiation, and surgery often do reduce tumor burden, these therapies do not change the underlying causes of the disease. Given the blatant failures of conventional cancer therapies, it is imperative that we examine optional and complementary therapies to assist the swelling ranks of American cancer patients. These therapies need to be considered earlier, rather than as a last resort by cancer patients.

The purpose of this protocol is to help cancer patients bridge critical gaps in their treatment programs so they can increase the odds of long-term disease remission. The information provided is based solely on peer-reviewed studies published in respected medical journals throughout the world. It is important for the reader to know that this protocol is based on the results of published research, as there are many fraudulent "cancer cures" that are not substantiated in the medical literature.

We call these "adjuvant" treatment recommendations because the primary therapy will inevitably be administered by the attending physician. The problem is that even the best oncologist may not be able to keep up with the latest findings because of the sheer volume of new treatment data. Our mission, therefore, is to provide insightful cancer-treatment information that is too often overlooked by practicing oncologists.

The Importance of "Measuring" Success or Failure

It is of critical importance in any cancer treatment program to measure success or failure. This can be accomplished in most cancers by evaluating tumor markers in the blood and/or by looking at the actual tumor(s) via medical imagery. When using any kind of cancer therapy, it is crucial that blood tumor marker tests be performed every 30 to 45 days. If the tumor markers reveal regression of the cancer, then existing therapy may be continued. If tumor markers indicate disease progression, then a different treatment approach should be implemented immediately. At the end of this protocol, we provide a listing of blood tumor marker tests as they relate to specific types of cancer.

An Overlooked Therapy

Many types of cancer cells use an enzyme called cyclooxygenase-2 (COX-2) to propagate. This includes cancers of the colon, pancreas, breast, prostate, bladder, lung, head and neck, to name a few. The good news is that COX-2 is also involved in the rheumatoid arthritis process, so there are drugs that are already approved to treat arthritis that may also be prescribed for cancer patients.

Drugs that inhibit the cyclooxygenase enzyme are known as COX-2 inhibitors. The two newest COX-2 inhibitors are Celebrex and Vioxx, but we suggest that cancer patients consider older drugs that have a more predictable safety history. One drug that oncologists may consider prescribing is Lodine XL, a drug used to treat arthritis that also interferes with COX-2 activity. A safer COX-2 inhibiting drug called nimesulide is sold in Europe but is not yet approved by the FDA.

Cancer cells often produce large amounts of COX-2 and use it as a biological fuel to cause rapid proliferation of cell division. An article in the journal Cancer Research (1999 March 1; 59 [5]:987-90) shows that COX-2 levels in pancreatic cancer cells are 60 times greater than in adjacent normal tissue. A handful of physicians knowledgeable about COX-2 and cancer are prescribing COX-2 inhibitors to their patients. It was back in 1997 that the Life Extension Foundation recommended the European drug nimesulide to cancer patients. The FDA has aggressively blocked the personal-use importation of this potential life-saving medication to cancer patients.

Scientists are now actively investigating COX-2 inhibitors as drugs that would be effective in both the prevention and treatment of many cancers. When COX-2 drugs are given to patients with colon polyps (precancerous lesions), the lesions completely disappear. When a group of rats were given a potent carcinogen, there was a 90% reduction in those who developed cancer if they were on COX-2 inhibition therapy. In the few rats that did develop the tumors while taking COX-2 inhibition therapy, the tumors were 80% smaller and less numerous than in the group not on COX-2 inhibition (Wall Street Journal, Sept. 7, 1999).

We predict that COX-2 inhibiting drugs will eventually be approved to treat cancer, but in the meantime, cancer patients should ask their doctors to consider prescribing a COX-2 inhibiting drug as an adjuvant therapy.

Drugs that inhibit COX-2

Lodine XL is an arthritis drug approved by the FDA that interferes with COX-2 metabolic processes. The maximum dosage for Lodine is 1000 mg daily. Everyone now appears to be using Lodine XL extended-release tablets for convenient once-a-day dosing. The Lodine XL 500-mg tablet enables physicians to prescribe the maximum dosage of Lodine XL-1000 mg per day-as two tablets in a single daily dose. As with any nonsteroidal anti-inflammatory drug (NSAID), extreme caution and physician supervision are a must.

The most common complaints associated with Lodine XL use relate to the gastrointestinal tract. Serious GI toxicity such as perforation, ulceration, and bleeding can occur in patients treated long term with NSAID therapy. Serious renal and hepatic reactions have been reported only rarely. Lodine XL should not be given to patients who have previously shown hypersensitivity to it or in whom aspirin or other NSAIDs induce asthma, rhinitis, urticaria, or other allergic reactions. Fatal asthmatic reactions have been reported in such patients receiving NSAIDs.

Nimesulide is a safer COX-2 inhibitor, but is not approved by the FDA. It is available from Mexican pharmacies or can be ordered by mail from European pharmacies. The suggested dose for nimesulide is two 100-mg tablets a day. It is important that your physician know you are taking nimesulide as an adjuvant cancer therapy. Please refer to the "molecular oncology" section of this protocol for a detailed description of the connection between COX-2 and cancer.

Why Many Cancer Patients Need Cholesterol-Lowering Drugs

The regulation of cancer cell growth is often governed by a family of proteins known as RAS oncogenes. The RAS family is responsible for modulating the regulatory signals that govern the cancer cell cycle and proliferation. Mutations in genes encoding RAS proteins have been intimately associated with unregulated cell proliferation (i.e., cancer).

There is a class of cholesterol-lowering drugs known as the "statins" that have been shown to inhibit the activity of RAS oncogenes. Some of these cholesterol-lowering "statin" drugs are lovastatin, simvastatin, and pravastatin.

The highest incidences of RAS mutations are found in cancers of the pancreas (90%), the colon (50%) and the lung; in thyroid tumors (50%), in liver tumors (30%), and in myeloid leukemia (30%). If you have one of these cancers, you should consider requesting an immunohistochemistry for the mutated RAS oncogene or a biopsied specimen in order to ascertain whether the combination of chemotherapy and a statin drug may be effective. (Information about obtaining RAS testing appears later in this protocol.)

As far as dosing is concerned, if the drug lovastatin (Mevacor) were chosen, a cancer patient with a mutated RAS oncogene should take as high as 80 mg a day for several months. Another approach is to take 80 mg a day of lovastatin for 3 weeks, take 2 weeks off, and then resume. It may be especially important to use a statin drug during chemotherapy. Statin drugs given with cytotoxic chemotherapy could provide the necessary one-two punch to kill a sufficient number of tumor cells for the patient to enter a period of long-term remission. Careful monitoring of liver enzymes is needed to guard against liver toxicity of the statin drugs. There are other potential side effects to watch out for, but in many cancers, statin drugs appear to be a powerful inhibitor of cancer cell proliferation. The "molecular oncology" section of this protocol provides more details about the use of statin drugs as an adjuvant cancer therapy.

Combining a COX-2 Inhibitor with a Statin

A novel approach would be to combine a "statin" drug such as lovastatin with a COX-2 inhibitor.

A study published in the journal Gastroenterology (1999, Vol. 116, No. 4, Suppl. A369) showed that lovastatin augmented by up to fivefold the cancer cell killing effect of a drug with COX-2 inhibiting properties (Sulindac). In this study, three different colon cancer cell lines were killed (made to undergo programmed cell death) by depriving them of COX-2. When lovastatin was added to the COX-2 inhibitor, the kill rate increased by up to fivefold.

Thus, those with certain cancers might benefit if their oncologists prescribed for several months 80 mg a day of Mevacor (lovastatin) and 1000 mg a day of Lodine XL.

Physician involvement is crucial to help protect against potential side effects of these drugs. Those who are concerned about potential toxicity should take into account the fact that the types of cancers these drugs might be effective against have extremely high mortality rates.

The Importance of Nutritional Support

Nutrition therapy helps to change the conditions in the body that favor tumor growth and return the cancer patient to a healthier status. More wellness in the body means less illness. Fungus grows on the bark of a tree due to the underlying conditions of heat, moisture, and darkness. One could "cut, burn, and poison" this fungus, but as long as the prevailing conditions of heat, moisture, and darkness were present, the fungal growth would return until the host was consumed. Similarly, a patient develops cancer due to a collection of conditions that compromise the host.

Nutrition is a low-cost, nontoxic, and scientifically validated adjuvant modality in the treatment of cancer. Adjuvant (helpful) nutrition and traditional oncology are synergistic, not antagonistic. Some reasons and rationale for using an aggressive nutrition program in comprehensive cancer treatment include

Avoiding malnutrition.
Reducing the toxicity of medical therapy, making chemotherapy and radiation therapy more selectively toxic to the tumor cells.
Stimulating immune function.
Selectively starving the tumor.
Providing biological response modifiers to assist mechanisms and improve outcomes in cancer therapy.

A complete nutritional support plan of action will be provided later in this protocol.

A Promising New Therapy

Angiogenesis (new blood vessel growth) is a key step in tumor growth, invasion, and metastasis. A substance that cuts the supply of blood to cancer cells can stop the primary tumor and its spread throughout the body. A new anti-angiogenesis cancer drug will enter human clinical trials in the United States at the end of 1999. The scientific literature shows that this drug induces a consistent and significant reduction in tumor growth in laboratory animals. In many cases the primary and metastatic cancer lesions are put into a dormant state and no longer propagate.

To date, a number of anti-angiogenesis agents have been identified. In animal models, treatment with angiogenesis inhibitors has proven anti-tumor effects. Early clinical experience with angiogenesis inhibitors indicates that optimal anti-angiogenesis therapy will likely be based on their long-term administration to cancer patients in adjunct to other therapies.

The published evidence indicates that the new angiogenesis-inhibitors offer great promise to cancer patients. The therapy is nontoxic and has shown efficacy against every type of cancer it has been tested against. One study showed that it suppressed metastatic tumor growth rates by 90%. Another study showed primary tumors regressing to become "dormant microscopic lesions."

Before raising any premature hope, we want to state that this new anticancer therapy consists of two drugs, endostatin and angiostatin. The FDA, however, is only permitting one of these two drugs (endostatin) to be used in the initial clinical trials. In other words, the FDA is not allowing terminally ill humans to use the two drugs that worked so remarkably well together in the animal studies. There is still reason to believe, however, that just one half of this drug combination (the endostatin) could save the lives of human cancer victims who have been sentenced to death by the medical establishment.

Those suffering from a nontreatable form of cancer should consider entering those clinical trials where endostatin, a potent angiogenesis-inhibiting drug, will be tested in humans. It is hoped that the other angiogenesis-inhibiting drug, angiostatin, will soon be added to endostatin in order to replicate the successful two-drug combo that so effectively treated cancer in the laboratory studies.

Primary and metastatic tumors require ongoing angiogenesis (new blood vessel formation) to support their growth. This is an undisputed fact based on today's understanding of oncological processes. Weak angiogenesis-inhibiting agents such as shark cartilage have not shown adequate efficacy. Angiostatin and endostatin are naturally produced proteins that shut off new blood vessel formation to tumors.

Angiostatin and/or endostatin have produced dramatic remissions in animal studies. Human cancer patients can access endostatin in FDA- sanctioned human clinical trials. The drug endostatin is derived from a protein found in the human body. In animal trials, the protein drug wiped out several forms of cancer by choking off the blood supply to tumors.

Although many cancer patients develop a resistance to conventional drugs, they aren't likely to do so with endostatin. What's more, the new natural treatment appears to stop cancer from spreading to other parts of the body.

So far, endostatin has worked only in mice. Now the National Cancer Institute in Frederick, MD, wants to find out whether the drug can starve human tumors. The initial trials are scheduled to begin at the University of Texas, M.D. Anderson Cancer Institute in Houston, and the University of Wisconsin's Comprehensive Cancer Center in Madison. The "molecular oncology" section of this protocol provides more detailed information about endostatin and angiostatin.

(To find out specific information about entering these clinical trials, you may call (800) 544-4440).

Protecting Against Chemotherapy Toxicity

Cancer patients using cytotoxic chemotherapy drugs should ask their oncologists to place them on FDA-approved immunoprotective drugs 1 week before the first chemotherapy drug is administered. Depending on the type of cancer and the chemotherapy regimen that will be used, two of the most important FDA-approved drugs to consider are Neupogen, a granulocyte-colony stimulating factor drug (G-CSF) and Leukine, a granulocyte-macrophage-colony stimulating factor (GM-CSF).

Neupogen and Leukine stimulate the production of T-lymphocytes, macrophages, and other immune cells which are valuable in preventing the toxic effects on the bone marrow during chemotherapy. These immune-protecting drugs enable chemotherapy to be given at a higher dose that may make it effective. Stimulated macrophages are powerful tumor killers, as has been demonstrated by clinical studies using interleukin-2 and GM-CSF, or G-CSF. In addition, colony growth factors are able to accelerate regeneration of blood cells following chemotherapy. Initial clinical experience with GM-CSF and G-CSF has shown that severe neutropenia (immune impairment) due to chemotherapy drugs may be prevented or at least decelerated, reducing the number of severe infections.

Alpha-interferon and interleukin-2 are immune cytokines (regulators) that should also be considered by cancer patients. Interferon directly inhibits cancer cell proliferation and has already been used in the therapy of hairy cell leukemia, Kaposi's sarcoma, and malignant melanoma. Interleukin-2 allows for an increase in the cytotoxic activity of Natural Killer (NK) cells. These drugs must be carefully administered by an oncologist, as they can produce temporary side effects.

Retinoic acid (vitamin A) analog drugs enhance the efficacy of some chemotherapy regimens and reduce the risk of secondary cancers. Ask your oncologist to consider prescribing vitamin A analog drugs such as Accutane. Again, the use and dosage of potentially toxic drugs such as Accutane must be carefully prescribed by your attending oncologist.

Some cancer patients produce too many T-suppressor cells that shut down optimal immune function. The administration of drugs such as cimetidine prevent cancer cells from prematurely shutting down the immune system. An immune cell subset blood test will reveal the status of your T-helper cells, T-suppressor cells, and natural killer cell count and activity.

The proper administration of Neupogen or Leukine prior to the initiation of chemotherapy can dramatically reduce the immune damage that chemotherapy inflicts on the body and increase the cancer cell killing efficacy of conventional chemotherapy drugs. Please remember that, so far, we have only talked about drugs that require physician administration. There are safe nutrients that can be self-administered that also protect against chemotherapy toxicity and immune impairment.

Some of these nutrients include Coenzyme Q10, which has been shown in several studies to protect against chemotherapy damage to the heart. CoQ10 was highlighted as the topic of professional medical discussion as a complementary treatment for cancer at a recent meeting (Oncology Hunting) 1999 Feb; 13 [2]:166). Natural vitamin E succinate has also been shown to protect organs throughout the body from the damaging effects of cytotoxic chemotherapy.

CAUTION: Some studies indicate that Coenzyme Q10 should not be taken at the same time as chemotherapy. If this is true, it would be disappointing, since 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 whether to take CoQ10 during chemotherapy.

Supplemental melatonin in doses of 10 to 40 mg a night can protect and restore normal blood-cell production caused by the toxicity of chemotherapy. A study was performed in 80 patients with metastatic solid tumors to evaluate the benefits of melatonin. Patients received either chemotherapy alone or chemotherapy plus 20 mg each night of melatonin. Thrombocytopenia was significantly less frequent in patients receiving melatonin. Other common side effects of cancer chemotherapy-such as malaise, asthenia, stomatitis, and neuropathy-occurred less frequently in patients receiving melatonin. This corroborated previous studies showing that the administration of melatonin during chemotherapy can prevent some side effects, especially myelosuppression (blood-cell production suppression) and neuropathy.

The administration of FDA-approved drugs such as Neupogen or Leukine are important to cancer patients, even though melatonin has similar mechanisms of action. There are too many published studies about the prophylactic benefits of these FDA-approved drugs for them not to be used prior to the administration of chemotherapy.

To treat low white blood cell counts, the FDA-approved drug Neupogen or Leukine may be considered by your immunologist or hematologist. Drugs such as Neupogen, Leukine, and Intron A alpha-interferon (an immune-modulating cytokine) can restore immune function debilitated by toxic cancer chemotherapy drugs. In one study, patients with refractory (resistant to treatment) solid tumors treated with standard chemotherapy and GM-CSF had a 33.3% objective response rate, versus 15% with chemotherapy alone. If you are on chemotherapy and your blood tests show immune suppression, you should demand that your oncologist use the appropriate immune restoration drug(s).

(Please refer to the Cancer Chemotherapy protocol for additional suggestions on protecting against the multiple toxicities these drugs can cause.)

Immuno-Histochemistry Testing

Cancer patients whose tumor cells have a mutant p53 oncogene are far more likely to benefit from certain therapies than are others. Only a pathology examination of the actual cancer cells can determine p53 status. An immunohistochemistry test can help to determine the p53 and RAS oncogene status of tumor cells. The following laboratory can perform this test:

IMPATH Laboratories

1010 Third Avenue, Suite 203

New York, N.Y. 10021

Phone: 1 (800) 447-5816

IMPATH Laboratories measures mutant p53. If the test is positive, you have mutant p53 and are more likely to benefit from products such as soy genistein. If the test is negative, it indicates that you have functional p53 and are less likely to benefit from soy extracts.

The Life Extension Foundation first recommended immunohistochemistry testing in 1997. An article that appeared in a September 1999 issue of the Lancet (1999; 354:896-900) showed that immunohistochemical detection aids in the diagnosis and staging of breast cancer and should become "a standard method of node examination in postmenopausal patients." While the Lancet study looked only at breast cancer cells, the Foundation continues to recommend that all cancer patients consider immunohistochemical testing of their tumor cells to determine p53, RAS, and other oncogene status

Integrated Cancer Therapy

With one in three Americans now using alternative medicine therapies regularly, many conventional oncologists are still not incorporating the published findings of nutritional science that benefit their patients' fight against cancer.

The Life Extension Foundation has researched an impressive collection of published studies showing that the disease process can be favorably mitigated with nutritional factors. These adjuvant treatments present approaches to boost immune system function, inhibit cancer cell division, induce cancer cells to differentiate back into mature cells, inhibit cancer cell metastases, prevent angiogenesis, and modulate the effect of hormones on cancer cell growth. These studies also reveal complementary methods for reducing the toxicity and the suppression of the immune system for both chemotherapy and radiation therapy.

It is impossible to completely describe all the mechanisms of action for the nutrients and hormones recommended in this Cancer Treatment protocol. What follows are discussion and studies that substantiate key recommendations of the protocol. The inclusion of certain nutrients in the following descriptions does not mean that they are more important than nutrients such as vitamin C and selenium, which are not discussed because of lack of space.

Many cancers require aggressive conventional therapies. The Life Extension Foundation has not found an effective alternative therapy that is sufficiently potent to shrink large primary or widely disseminated cancer. Treatment of such advanced tumors may yet require conventional therapies such as chemotherapy, radiation therapy, and surgery. The conventional approach to cancer using one or more of the big three can leave the patient's immune system suppressed and can induce a catabolic (or wasting) state with rapid weight loss. Cancer patients should insist that their oncologists accept their desire to support their immune systems with nutritional therapies and the benefits of using such protocols to assist the conventional medicine.

Continued Testing and Monitoring Is Crucial

The Foundation emphasizes the importance of regular tumor marker testing to measure and monitor cancer status and therapy. Patients should establish with their doctors a planned schedule for cancer testing to monitor their progress during treatment. Modern testing is one of the most important tools for combating cancer, and both the patient and the doctor should be cognizant of the latest testing methods and should establish a monthly or regular testing schedule. Some cancers will require x-ray, MRI, or CAT scans to be detected and/or monitored, while other cancers can be monitored using blood tumor markers. For cancers that do not have an established blood tumor marker test, patients should use MRI, CAT scans, and other imaging diagnostics every 30 to 60 days to determine whether tumor shrinking is actually occurring and to measure the progress of any remissions seen.

Nutritional Therapies

Patients who have been diagnosed with large primary tumors may have to rely on conventional cancer therapy to treat the primary tumor, however, the nutrient and hormone adjuvant therapies presented in this book may help control metastasized cancer cells and reduce the toxicity of chemotherapy and radiation therapy. It should be noted that nutritional therapy is a long-term therapy requiring consistent and proper use of nutritional supplements and the measuring of cancer status (via regular blood testing) to determine the patient's response. The use of nutritional support is gaining in popularity because of high public demand and scientific findings.

Chemotherapy has a poor overall record of success over the past 30 years, but the Life Extension Foundation has identified adjuvant therapies to augment chemotherapies by making these drugs less toxic to healthy cells and more toxic to cancer cells, and by reducing the suppression of the immune system.

It should be noted that many cancer patients turn to alternative therapy fairly late in the course of the disease. Under such circumstances, and after the failure of conventional medicine, the prognosis for a cure is poor and the best many patients can hope for is an increased survival rate and reduced pain. In many cases, the failure of alternative medicine at the latest stages of cancer is used as a political statement by the medical establishment on the general topic of alternative therapies for cancer therapy. Keep in mind that conventional medicine has, in most cases, failed to offer any improvement or hope for the majority of desperate patients with advanced-stage cancers.

The Science Behind Cancer Nutrition Therapies

Finnish oncologists used high doses of nutrients along with chemotherapy and radiation for lung cancer patients. Normally, lung cancer is a "poor prognostic" malignancy advanced with a 1%-2% expected survival at 30 months under normal treatment. In this study, however, 8 of 18 patients (44%) were still alive 6 years after therapy.

Oncologists at West Virginia Medical School randomized 65 patients with transitional cell carcinoma of the bladder into either the "one-per-day" vitamin supplement providing the RDA, or a group which received the RDA supplement plus 40,000 IU of vitamin A, 100 mg of B6, 2000 mg of vitamin C, 400 IU of vitamin E, and 90 mg of zinc. At 10 months, tumor recurrence was 80% in the control group (RDA supplement) and 40% in the experimental "megavitamin" group. Five-year projected tumor recurrences were 91% for controls and 41% for "megavitamin" patents. Essentially, high-dose nutrients cut tumor recurrence in half.

In a nonrandomized clinical trial, Drs. Hoffer and Pauling instructed patients to follow a reasonable cancer diet (unprocessed food low in fat, dairy, and sugar), coupled with therapeutic doses of vitamins and minerals. All 129 patients in this study received concomitant oncology care. The control group of 31 patients who did not receive nutrition support lived an average of less than 6 months. The group of 98 cancer patients who did receive the diet and a supplement program was categorized into three groups:

Group 1:	Poor responders or approximately 20% of treated group. These had an average lifespan of 10 months or a 75% improvement over the control group.
Group 2:	Good responders, or approximately 47%, who had various cancers including leukemia, lung, liver, and pancreas; had an average lifespan of 72 months (6 years).
Group 3:	Good female responders or approximately 32% with involvement of reproductive areas (breast, cervix, ovary, uterus); group 3 had an average lifespan of over 10 years. Many were still alive at the end of the study.

In examining the diet and lifespan of 675 lung cancer patients over the course of 6 years, researchers found that the more vegetables consumed, the longer the lung cancer patient lived.

In 200 cancer patients studied who experienced "spontaneous regression," 87% made a major change in diet, mostly vegetarian in nature, 55% used some form of detoxification, and 65% used nutritional supplements.

Researchers at Tulane University compared survival in patients who used the macrobiotic diet versus patients who continued with their standard western lifestyle. Of 1467 pancreatic patients who made no changes in diet, 146 (10%) were alive after one year, while 12 of the 23 matched pancreatic patients (52%) consuming macrobiotic foods were still alive after one year.

Benefits of Genistein

Genistein has shown significant cell-inhibiting effects in many different types of cancer. A study was conducted to examine the role genistein played in growth factors'-such as protein tyrosine kinase and in thymidine incorporation into cancer cells. Genistein suppressed protein tyrosine kinase activity and the subsequent growth stimulatory incorporation of thymidine into cancer cells. The scientists speculated that genistein has potential value in the prevention and treatment of some tumors in vivo.

In other studies, genistein has shown anti-angiogenesis properties, cancer cell adhesion-inhibition properties, estrogen-receptor blocking properties, and apoptosis-inducing effects. An investigation into the effect of soy genistein on the growth and differentiation of human melanoma cells showed that genistein significantly inhibited cell growth. Some studies suggest that genistein may enhance the efficacy of certain chemotherapy regimens.

Soy protein contains several anticancer agents including genistein and other isoflavones. In one study, a lower incidence of prostate cancer was shown in Chinese men who had higher amounts isoflavonoid phytoestrogens, daidzein, and equol within their prostatic fluids and in their blood plasma. The study concluded that the high concentrations of isoflavones present in the prostatic fluid of Asian men may protect them from prostate disease.

A study in a 1999 issue of the Journal of Nutrition reported that "dietary soy products may inhibit prostate tumor growth through a combination of direct effects on tumor cells and indirect effects on tumor neovasculature." Earlier in 1999, a study in the British Journal of Cancer reported an inhibitory effect of genistein and quercetin on the growth of tumors.

Curcumin and genistein have both been shown to inhibit the growth of estrogen-positive human breast cancer cells induced by pesticides. When curcumin and genistein were added to breast cancer cells, a synergistic effect resulted in a total inhibition of cancer cell growth caused by pesticide-induced estrogenic activity. This study suggested that the combination of curcumin and genistein in the diet has the potential to reduce the proliferation of estrogen-positive cells induced by mixtures of pesticides or estrogen. Since it is difficult to remove pesticides completely from the diet, and since neither curcumin nor soy genistein is toxic to humans, their inclusion in the diet in order to prevent hormone-related cancers deserves consideration. Curcumin appears to function via several different mechanisms to inhibit cancer cell proliferation.

Differentiation-inducing agents such as genistein, retinoids, and vitamin D analogs inhibited tumor cell-induced angiogenesis in vitro and in vivo. Simultaneous administration of retinoids and 1,25-dihydroxy vitamin D3 led to a synergistic inhibition of tumors associated with angiogenesis in mice. Recently, these compounds have been shown to induce and act in concert with natural angiogenic inhibitors such as interferons.

A study was conducted to determine whether genistein could induce human breast adenocarcinoma cell maturation and differentiation. Treating these cells with genistein resulted in growth inhibition accompanied by increased cell maturation. These maturation markers were optimally expressed after 9 days of treatment with genistein. Both estrogen-receptor-positive and estrogen-receptor-negative cells became differentiated in response to genistein, which is a crucial step in inducing cancer cell apoptosis (programmed cell death). Despite this study, we do not recommend that women with estrogen-receptor-positive breast cancer use soy genistein because of the following evidence.

Genistein appears to be especially effective against prostate cancers. One study showed that genistein inhibited the proliferation and expression of the in vitro invasive capacity of tumoral prostatic cells. In a cell culture system, genistein appeared to be cytotoxic and inhibitory to PC-3 cells. The more aggressive the prostate cancer cell culture studies, the more effective was the genistein, both with respect to proliferation rate and inhibition of growth factors.

More recently, the Japanese Journal of Cancer Research (1999 April; 90 [4]:393-98) reported results of a comprehensive rat study which provides further evidence that soybean isoflavones have a potential as chemopreventive agents against carcinogenesis in the prostate.

Other investigators have reported anticancer effects of genistein on lung cancer in the 1999 Journal of Nutritional Cancer, where researchers reported a specific effect on lung cancer cells.

Breast Cancer and Genistein

One study tested the effects of naturally occurring flavonoids on the proliferation of an estrogen-receptor-positive human breast cancer cell line. Genistein inhibited cell proliferation, but this effect was reversed when estrogen was added. The flavonoids hesperidin, naringenin, and quercetin inhibited breast cancer cell proliferation even in the presence of high levels of estrogen. These flavonoids apparently exert their antiproliferative activity via a mechanism that is different from that of genistein. Women with any type of breast cancer should test their serum estrogen levels to make sure that too much estrogen is not present if they are taking high doses of soy. Estrogen can combine with the phytoestrogen genistein to cause some breast cancer cells to grow faster. Other studies, however, show that genistein blocks certain types of estrogen receptor sites, thus inhibiting the proliferation of these types of breast cancer cells.

CAUTION: The Foundation has made a preliminary determination that women with estrogen-receptor-positive breast cancer should not take soy supplements based on evidence that an estrogenic growth effect could occur in some forms of estrogen-receptor-positive breast cancer. Until more is known about the effects of soy phytoestrogens in this type of cancer, compounds such as genistein should be avoided in those with estrogen-receptor-positive breast cancer.

Summing up the possible benefits of genistein and other natural therapies is a May 1999 study in the North American Urological Clinical Journal regarding findings of new nontoxic cancer therapies. Researchers reported, "Other agents that promise low toxicity include vitamin D and its analogs, genistein and related isoflavones, green tea polyphenols, and retinoic acid analogs."

Information on how cancer patients should use soy genistein appears at the end of this protocol. The Foundation reiterates that regular testing is recommended for all cancer patients to measure the status and progression of the cancer and the trend of any protocol used; i.e., if tumor markers elevate for 30 to 60 days after beginning soy extract supplementation, discontinue use and seek another therapy immediately.

Benefits of Green Tea

Green tea is the staple beverage of the Japanese and Chinese cultures. It contains a chemical known as epigallocatechin gallate, which is one of the polyphenolic catechins, a family of chemicals many times more potent against free radicals than vitamin E. In a study to measure the effect of green tea consumption in Japanese populations, it was found that green tea had a "preventative effect against cancer among humans." This study surveyed 8552 people over a 9-year period (71,248 person years) and found that cancer incidence was low for those people who consumed green tea regularly. The study also found that the more green tea was consumed, the lower the risk of cancer. Many women interviewed for the study consumed more than 10 cups of green tea daily, and their cancer incidence was the lowest in the study. The overall consumption of green tea correlated with both men and women.

University Hospitals of Cleveland researchers reported in the May 1999 Journal of Urological Oncology that prostate cancer (PC) is the second leading cause of cancer-related deaths among males in the United States. According to an estimate, 1 of every 11 American men will eventually develop PC. Researchers suggested that one way to reduce the occurrence of cancer is through natural chemoprevention. PC represents an excellent candidate disease for chemoprevention because it is typically diagnosed in men over 50 years of age, and therefore even a modest delay in neoplastic development achieved through pharmacological or nutritional intervention could result in a substantial reduction in the incidence of clinically detectable disease. The ideal agent(s) suitable for chemoprevention of PC should be the one(s) with proven efficacy in the laboratory experiments on one hand, and with proven epidemiological basis on the other hand. This review attempts to address the issue of possible uses of tea, especially green tea, for the prevention of PC.

The researchers provided an experimental as well as an epidemiological basis for this possibility. They also pointed out that many laboratory experiments conducted in cell culture systems and in animal models have shown the usefulness of green tea and the polyphenols present in it-against PC.

The epidemiological basis for this possibility is twofold. First, some epidemiological observations have suggested that people who consume tea regularly have a lower risk of PC-related deaths. Second, the incidence of PC in China, a population that consumes green tea on a regular basis, is the lowest in the world (Semin. Urol. Oncol., 1999 May; 17 [2]:70-76).

Another study reported in the July 1999 Japanese Journal of Cancer Research further substantiated the benefits of green tea against specific cancer cells. Researchers emphasized its role in the prevention and treatment of cancers such as stomach cancer.

Investigators reported in the September 1999 American Journal of Clinical Nutrition that "herbal teas inhibit mevalonate synthesis and thereby suppress cholesterol synthesis and tumor growth," further supporting the section in this protocol which discusses the reduction of cholesterol in the fight against cancer (Am. J. Clin. Nutr., 1999 Sept; 70 [3 Suppl]:491S-99S).

A study found that apoptosis occurred in prostate cancer cell lines LNCaP, PC-3, and DU125 in response to green tea extract. The cancer cell morphology and DNA fragmentation were induced by the most active constituent of green tea, epigallocatechin gallate (EGCG). The study concluded that EGCG triggered apoptosis (programmed cell death) in human prostate cancer cells.

Another study found that two phenols contained in green tea extract had inhibitory effects on several cancer cell lines including lung, stomach, and mammary cancers. It was found that the phenols, epigallocatechin (EGC), and epicatechin gallate (ECG) inhibited the growth of human lung cancer cell PC-9.

Collectively, the results indicate that tea possesses anticarcinogenic activity in the colon, and this most likely involves multiple inhibitory mechanisms (Proc. Soc. Exp. Biol. Med., 1999 April; 220 [4]:239-43).
A review published in a 1999 issue of Experimental Biological Medicine summarizes the mechanisms of action of green teas as follows:

Tea polyphenols are powerful antioxidants that may play a role in lowering the oxidation of LDL-cholesterol, with a consequent decreased risk of heart disease, and may also diminish the formation of oxidized metabolites of DNA, with an associated lower risk of specific types of cancer.
Tea and tea polyphenols selectively induce Phase I and Phase II metabolic enzymes that increase the formation and excretion of detoxified metabolites of carcinogens.
Tea lowers the rate of cell replication and thus the growth and development of neoplasms.
Tea modifies the intestinal microflora, reducing undesirable bacteria and increasing beneficial bacteria. The accumulated knowledge suggests that regular tea intake by humans might provide an approach to decreasing the incidence of and mortality from major chronic diseases.

Benefits of Garlic

Epidemiological studies in China have provided reasons to suspect that a rich garlic content in the diet might reduce the proliferation of tumors in humans. Researchers reported in the March 1999 issue of Phytomedicine relative to experiments conducted on human tumor cell lines to determined the influence of garlic to inhibit the growth of human liver or colon cancer cell lines. Results suggest a strong antiproliferative effect of garlic on human cancer cells (Phytomedicine, 1999 Mar; 6 [1]:7-11).

Although the herb garlic by itself possesses these medical properties, aged garlic extract (AGE) has additional benefits due to tightly controlled manufacturing. The process of cold-aging garlic may enhance its medicinal factors, and the aging process also reduces the tendency of garlic to irritate the digestive tract.

A study investigated aged garlic extract in an effort to determine whether it could inhibit proliferation of cancer cells. The proliferation and viability of erythroleukemia and hormone-responsive breast and prostate cancer cell lines were evaluated. The erythroleukemia cells were not significantly affected by the garlic extract, but the breast and prostate cancer cell lines clearly were susceptible to the growth-inhibitory influence of aged garlic extract. The antiproliferative effect of aged garlic extract was limited to actively growing cells. This study provided evidence that garlic can exert a direct effect on established cancer cells.

A Chinese study revealed that garlic effectively prevented oral precancer and oral cancer cell proliferation (Hunan I Ko Ta Hsueh Hsueh Pao, 1997; 22 [3]:246-48).

There is a debate among alternative doctors as to whether aged "odorless" garlic is better than high-allicin garlic supplements. For those fighting cancer on an acute basis, perhaps both forms of garlic should be considered. Specific garlic dosing suggestions are provided at the end of this protocol.

Benefits of Vitamin A and Vitamin D

Nutrients with an inhibitory effect on cancer-cell proliferation include vitamin A (and synthetic vitamin A analogs). The best example of the effectiveness of vitamin A and beta-carotene in inhibiting cell proliferation is with patients who suffer from cancer of the mouth. Vitamin A or beta-carotene supplementation may induce a remission in early stage I mouth cancer as long as these nutrients continue to be consumed. A similar study of 44 patients with mouth lesions caused by chewing tobacco found that spirulina's (chlorella) high concentration of beta-carotene also proved effective for 20 patients after one year.

Vitamin D3 and its analogs may inhibit cancer cell growth and induce cancer cells to differentiate back into normal cells. An experimental study was performed on a prostate cancer cell line, PC-3, to measure the effect of a vitamin D analogue. A control medium was conducted in parallel. Cell proliferation was measured at 7 and 12 days, and it was found that results "were dose dependent varying from 40 to 70% of controls." The maximum inhibitory effect was at 0.1 micromol/L; however, the study found that "longer incubation times" were more effective than high concentrations of the vitamin D analog. The study concluded that vitamin D deficiency increased the risk of prostate cancer.

The vitamin D analog was used in another study of MCF-7 breast cancer cells grafted into nude mice to determine whether vitamin D could mediate apoptosis of breast cancer in vivo. Two delivery methods were used to administer the vitamin D time release pellets and daily injections. At 4 weeks the volume of tumors was reduced fourfold versus the control group. Characteristic "apoptotic morphology" was observed at 5 weeks with MCF-7 tumor cells showing a sixfold increase in DNA fragmentation measured by in situ labeling. The study found that vitamin D demonstrated apoptotic morphology and regression of human breast tumors and that the study "supported the concept that vitamin D compounds can effectively target human breast cancer."

CAUTION: Both vitamin A and vitamin D can have toxic effects in high doses. Consult with health care professionals before increasing doses of either vitamin to high levels.

Benefits of EPA Fish Oil

Fish oil may enhance the effectiveness of cancer chemotherapy drugs. A study compared different fatty acids on colon cancer cells to see whether they could enhance mitomycin C, a chemotherapy drug. The fish oil containing high amounts of eicosapentaenoic acid (EPA) was shown to sensitize colon cancer cells to mitomycin C. Fish oil has been shown to specifically induce apoptosis of pancreatic cancer cells and to inhibit metastasis of breast and lung cancer cells.

A June 1999 study demonstrated the benefits of EPA in reducing acute protein phase response which leads to wasting in cancer patients. Researchers indicated that "the presence of an acute-phase protein response has been suggested to shorten survival and contribute to weight loss in patients with pancreatic cancer. The acute-phase protein response tends to progress in untreated patients but may be stabilized by the administration of a fish oil-enriched nutritional supplement. This may have implications for reducing wasting in such patients" (Journal of Nutrition, 1999 June; 129(6):1120-25).

Other studies have found that EPA induced alternations of the fatty-acid composition of cancer cells, which made them more vulnerable to the chemotherapy effects. Although preliminary, these findings imply that EPA specifically enhances the chemosensitivity of malignant cells.

Conjugated Linoleic Acid (CLA)

CLA has been shown both in vitro and in animal models to have strong antitumor activity. An early protective effect was noted in one study that focused on the maturation of mammary cells, and the study concluded that "exposure to CLA during Y-maturation may modify the development of Y-target cells that are normally susceptible to carcinogen-induced transformation."

Investigators at Roswell Park Cancer Institute in Buffalo, New York, conducted rat studies and reported inhibited breast cancer cell outgrowth using CLA (Exp. Cell. Res., 1999 July 10; 250 [1]:22-34).
Another study investigated the effect of dietary CLA on the growth of human breast adenocarcinoma cells in immunodeficient mice. Similarly it was found that CLA inhibited the development and growth of mammary tumors. Moreover, CLA completely abrogated the spread of breast cancer cells to lungs, peripheral blood, and bone marrow. These results indicate the ability of dietary CLA to block both the local growth and systemic spread of human breast cancer via mechanisms independent of the host immune system.

CLA has been shown to inhibit initiation and promotion stages of carcinogenesis in several experimental animal models. A study of mice with skin tumors showed that CLA inhibited tumor yield. This study confirmed previous studies showing that CLA inhibits tumor promotion in a manner that is independent of its cancer-prevention effects.

Benefits of Echinacea

The popularity of echinacea has grown during the last couple of years because of its ability to enhance the immune system, especially during the cold and flu season. However, echinacea also has profound anticancer effects related to its ability to increase NK cell activity, which was improved by 221% in one study of patients suffering from metastasized cancers of the colon and esophagus. Another naturally occurring chemical found in echinacea (arabinogalactan) is known to stimulate macrophages' B tumor killing cells.

Benefits Whey Protein

Whey protein concentrate has been studied for cancer prevention and treatment. When different groups of rats were given a powerful carcinogen, those fed whey protein concentrate showed fewer tumors and a reduced pooled area of tumors. The researchers found that whey protein offered "considerable protection to the host" over that of other proteins, including soy.

At low concentrations, whey appears to inhibit the growth of breast cancer cells. One clinical study with cancer patients showed a regression in some patients' tumors when they were fed whey protein concentrate at 30 grams per day. As noted in a related protocol (but worth repeating in this context), this discovery led researchers to discover a relationship between cancerous cells, whey protein concentrate, and glutathione. Glutathione is an antioxidant that protects the body against harmful compounds. It was found that whey protein concentrate selectively depletes cancer cells of their glutathione, thus making them more susceptible to cancer treatments such as radiation and chemotherapy.

It has been found that cancer cells and normal cells will respond differently to nutrients and drugs that affect glutathione status. What is most interesting is that the concentration of glutathione in tumor cells is higher than that of the normal cells that surround it. This difference in glutathione status between normal cells and cancer cells is believed to be an important factor in cancer cells' resistance to chemotherapy. As the researchers put it, "Tumor cell glutathione concentration may be among the determinants of the cytotoxicity of many chemotherapeutic agents and of radiation, and an increase in glutathione concentration in cancer cells appears to be at least one of the mechanisms of acquired drug resistance to chemotherapy."

They further state, "It is well known that rapid glutathione synthesis in tumor cells is associated with high rates of cellular proliferation. Depletion of cancer cell glutathione in vivo decreases the rate of cellular proliferation and inhibits cancer growth." The problem is, it's difficult to reduce glutathione sufficiently in tumor cells without placing healthy tissue at risk and putting the cancer patient in a worse condition. What is needed is a compound that can selectively deplete the cancer cells of their glutathione while increasing, or at least maintaining, the levels of glutathione in healthy cells. This is exactly what whey protein appears to do.

This research found that cancer cells subjected to whey proteins were depleted of their glutathione, and their growth was inhibited, while normal cells had an increase in glutathione and increased cellular growth. These effects were not seen with other proteins. Not surprisingly, the researchers concluded, "Selective depletion of tumor cell glutathione may in fact render cancer cells more vulnerable to the action of chemotherapy and eventually protect normal tissue against the deleterious effects of chemotherapy." The exact mechanism by which whey protein achieves this is not fully understood, but it appears that it interferes with the normal feedback mechanism and regulation of glutathione in cancer cells. It is known that glutathione production is negatively inhibited by its own synthesis. Since baseline glutathione levels in cancer cells are higher than those of normal cells, it is probably easier to reach the level of negative-feedback inhibition in the cancer cells' glutathione levels than in the normal cells' glutathione levels.
(See the Benefits of Whey Protein section of the Cancer Chemotherapy protocol.)

Benefits of melatonin

The evidence continues to mount that melatonin may be an effective adjuvant cancer therapy because melatonin boosts immune system function, suppresses free radicals, inhibits cell proliferation, and helps to change cancer cells back into normal cells.

A randomized study of 70 patients with advanced nonsmall lung cancer was conducted using chemotherapy (cisplatin) and melatonin support to measure immune system improvement during chemotherapy. The study was conducted using the World Health Organization specifications for clinical response and toxicity, and it was found that "chemotherapy was well tolerated in patients receiving melatonin and, in particular, the frequency of myelosuppression, neuropathy, and cachexia was significantly reduced in the melatonin group." The study concluded that chemotherapy with 20 mg daily of melatonin may improve the chemotherapy particularly with respect to the patient's survival time and the mitigating effect of "chemotherapeutic toxicity" for patients with advanced non-small cell lung cancer. This same hospital facility conducted a melatonin survey (several different but related cancer studies using the same dosage of melatonin = 20 mg/daily) that found similar results for patients being treated with the chemotherapy drugs mitoxantrone, cisplatin, etoposide, and 5-fluorouracil.

A 1999 Slovak research study regarding the use of melatonin in the treatment of tumors reported that "melatonin has potentially important influence on the neoplastic growth and direct and indirect oncostatic effect in some forms of neoplasia. The beneficial influence of melatonin alone or its combination with immunotherapy, radiotherapy, or chemotherapy in many clinical studies in patients with tumors was demonstrated" (Cesk. Fysiol., 1999 Feb; 48 [1]:27-40).

Another 1999 study in the Mutagenesis Cancer Journal (1999 Jan; 14 [1]:107-12) confirmed that melatonin is able to modulate and reduce chromosome damage by its involvement in regulating adverse oxidative stress and processes, thereby reducing DNA damage. In particular, researchers reported that melatonin is able to decrease damage at the chromosomal level.

Combining Melatonin with Interleukin-2

Melatonin has been seen to enhance the anti-cancer action of interleukin-2 (IL-2) and to reduce IL-2 toxicity. Melatonin use in association with IL-2 cancer immunotherapy has been shown to have the following actions:

Amplification of IL-2 biological activity by enhancing lymphocyte response and by antagonizing macrophage-mediated suppressive events.
Inhibition of production of tumor growth factors, which stimulate cancer cell proliferation by counteracting lymphocyte-mediated tumor cell destruction.
Maintenance of a circadian rhythm of melatonin, which is often altered in human neoplasms and influenced by cytokine exogenous injection.

The subcutaneous administration of 3 million IU a day of interleukin-2 (IL-2) and high doses of melatonin (40 mg a day orally) in the evening has appeared to be effective in tumors resistant either to IL-2 alone or to chemotherapy. The dose of 3 million IU a day of interleukin-2 is a low dose, while serious toxicity normally begins at 15 million IU a day. At present, 230 patients with advanced solid tumors and life expectancy less than 6 months have been treated with this melatonin/IL-2 combination. Objective tumor regressions were experienced in 44 patients (18%), mainly in patients with lung cancer, hepatocarcinoma, cancer of the pancreas, gastric cancer, and colon cancer. A survival longer than one year was achieved in 41% of the patients. The preliminary data show that melatonin synergizes with tumor necrosis factor (TNF) and alpha-interferon by reducing their toxicity.

Importance of Vegetables

Indole-3-carbinol (I3C), isothiocyanate, and sulforaphane are phytochemicals found in cruciferous vegetables. They have an inhibitory effect on cancer cell proliferation.

Sprague-Dawley rats were subjected to 7,12-dimethylbenzanthracene-(DMBA) induced mammary tumors in a study to report on antitumorigenic activity of di-indolylmethane (DIM), an acid B catalyzed metabolite of I3C that is formed in the intestines. The study found that DIM inhibited the proliferation of MCF-7 cells and that DIM (at 5 mg/kg every other day) inhibited the mammary tumor growth induced by DMBA. The study concluded that DIM metabolized from the phytochemicals of cruciferous vegetables presents a new class of relatively nontoxic Y antiestrogens that inhibit E2-dependence without affecting normal cells.

Can nutrition Help the Malnourished Cancer Patient?

A position paper from the American College of Physicians published in 1989 basically stated that total parenteral nutrition (TPN) had no benefit on the outcome of cancer patients. Unfortunately, this article excluded malnourished patients, which is bizarre, since TPN only treats malnutrition, not cancer. Most of the scientific literature shows that weight loss drastically increases the mortality rate of most types of cancer, while also lowering the response to chemotherapy. Chemotherapy and radiation therapy are sufficient biological stressors to induce malnutrition by themselves.

In the early years of oncology, it was thought that one could starve the tumor out of the host. Pure malnutrition (cachexia) is responsible for at least 22% and up to 67% of all cancer deaths. Up to 80% of all cancer patients have reduced levels of serum albumin, which is a leading indicator of protein and calorie malnutrition. Dietary protein restriction in the cancer patient does not affect the composition or growth rate of the tumor, but does restrict the patient's well being.

Parenteral feeding improves tolerance to chemotherapeutic agents and immune responses. One study indicated that malnourished cancer patients who were provided TPN had a mortality rate of 11%, while the group without TPN feeding had a 100% mortality rate. Preoperative TPN in patients undergoing surgery for GI cancer provided general reduction in the incidence of wound infection, pneumonia, major complications, and mortality. Patients who were the most malnourished experienced a 33% mortality and 46% morbidity rate, while those patients who were properly nourished had a 3% mortality rate with an 8% morbidity rate.

In 20 adult hospitalized patients on TPN, the mean daily vitamin C needs were 975 mg/day, which is over 16 times the RDA. Of the 139 lung cancer patients studied, most tested deficient or scorbutic (clinically vitamin-C deficient). Another study of cancer patients found that 46% tested scorbutic while 76% were below acceptable levels for serum ascorbate. Experts now recommend the value of nutritional supplements, especially in patients who require prolonged TPN support. Remember that 40% or more of cancer patients actually die of malnutrition, not from the cancer, according to medical experts. Nutrition therapy is the only treatment for malnutrition.

Properly nourished patients experience less nausea, malaise, immune suppression, hair loss, and organ toxicity than patients on routine oncology programs. Antioxidants such as beta-carotene, vitamin C, vitamin E, and selenium appear to enhance the effectiveness of chemotherapy, radiation, and hyperthermia while minimizing damage to the patient's normal cells. Protecting healthy cells thus makes these conventional therapies more of a "selective toxin."

An optimally nourished cancer patient can better tolerate the rigors of cytotoxic therapy. While, in simplistic theory, vitamin K might inhibit the effectiveness of anticoagulant therapy (Coumadin), vitamin K actually seems to augment the antineoplastic activity of Coumadin. In a study with human rheumatoid arthritis patients being given methotrexate, folic acid supplements did not reduce the antiproliferative therapeutic value of methotrexate. Tumor-bearing mice fed high doses of vitamin C (antioxidant), along with the pro-oxidant chemotherapy drug adriamycin, had a prolonged life and no reduction in the tumor-killing capacity of adriamycin. Lung cancer patients who were provided antioxidant nutrients prior to, during, and after radiation and chemotherapy had enhanced tumor destruction and significantly longer lifespan. Some of the benefits of complimentary nutrition therapy include the following:

Improved tolerance to radiation therapy.

Tumor-bearing mice fed high doses of vitamin C experienced an increased tolerance to radiation therapy without reduction in the tumor-killing capacity of the radiation.

Improved tolerance to cytotoxic chemotherapies.

In both human and animal studies, nutrients improve the host tolerance to cytotoxic medical therapies while allowing for unobstructed death of tumor cells. Nutrition therapy makes medical therapy more of a selective toxin on the tumor issue.

Bolstering immune functions.

We must rely on the capabilities of the 20 trillion cells that make up an intact immune system to find and destroy the undetectable cancer cells that inevitably remain after medical therapy. There is an abundance of data linking nutrient intakes to the quality and quantity of immune factors that fight cancer.

Selectively starve the tumor.

Tumors are primarily obligate glucose metabolizers, meaning "sugar feeders." Americans not only consume about 20% of their calories from refined sucrose, but often manifest poor glucose tolerance curves due to stress, obesity, low chromium and fiber intake, and sedentary lifestyles. Since this topic is of crucial importance, further information on how the cancer patient should properly regulate glucose will follow.

Providing antiproliferative factors.

Certain nutrients such as selenium, vitamin K, vitamin E, the fatty acid EPA, melatonin, and CoQ10 appear to have the ability to slow down the unregulated growth of cancer. Various nutritional factors-including vitamins A, D, and E; folic acid; bioflavonoids; and soybeans-have been shown to alter the genetic expression of tumors.

Cancer is "a Sugar Feeder"

Nobel laureate Otto Warburg, Ph.D., discovered in 1955 that cancer cells primarily use glucose for fuel, with lactic acid being an anaerobic by- product. Lactic acid buildup then generates a lower pH, fatigue, and enlarged liver (where lactic acid is converted back to pyruvate in the Cori cycle). Cancer causes a breakdown in normal energy metabolism, which is one of the reasons why so many cancer patients die of malnutrition or cachexia.

Since Warburg's pivotal study was published in a 1956 issue of the journal Science, other research has shown that the glucose utilization rate is high in neoplastic tissues. Glucose is, in fact, the preferred energy substrate for cancer cells, utilized mainly via the anaerobic glycolytic pathway. The large amount of lactates produced by this process is then transported to the liver where it is converted to glucose, thus contributing to further increase the host's energy wasting.

Interfering with carbohydrate and/or energy metabolisms could preferentially impair the malignant cells. Studies show that in vivo consumption of glucose by neoplastic tissues is very high. It is well known that the brain is one of the highest consumers of glucose among the normal tissues. Hepatomas and fibrosarcomas have been shown to consume roughly as much glucose as the brain does, and more prevalent carcinomas consume about twice as much.

One study showed lactate levels to be 27 to 83% higher in cancer patients than in related controls. If cancer cells use glucose through anaerobic fermentation, then lactic acid must accumulate as the inefficient by-product of energy metabolism. Hence, cancer therapies need to take into consideration the importance of regulating blood glucose levels.

Another study on ten healthy human volunteers assessed fasting blood glucose levels and the phagocytic index of neutrophils. Glucose, fructose, sucrose, honey, and orange juice all significantly decreased the capacity of neutrophils to engulf bacteria as measured by the slide technique. Starch ingestion did not have this effect. One epidemiological study showed that the risk associated with the intake of sugars, independent of other energy sources, more than doubled for biliary tract cancer in older women. Other studies show a correlation between breast cancer mortality and sugar consumption.

Starving Cancer
In his book Beating Cancer with Nutrition, Dr. Patrick Quillin makes specific recommendations about how glucose modulation can be utilized to help the cancer patient. Some of his recommendations include

Diets designed to lower glycemic index to regulate rises in blood glucose, hence selectively starving the cancer cells.
Low glucose total parenteral nutrition (TPN) solution.
Avocado extract (mannoheptulose) which inhibits glucose uptake in cancer cells.
Systemic Cancer Multistep Therapy, which injects glucose into the cancer patient to induce rapid malignancy growth then uses hyperthermia to selectively destroy the rapidly dividing cells.

Dr. Quillin provides a compelling case for the role of glucose in the growth and metastasis of cancer cells. According to Dr. Quillin, a frequent characteristic of many tumors is a high rate of glucose consumption along with an increase in anaerobic glycolysis (the conversion of glucose to lactase). By manipulating glucose levels, cancer cells can be starved over an extended time, or, conversely, glucose can be injected into the patient when a therapy is being utilized that targets rapidly dividing cells.

Glucose modulation therapy is an underutilized component in the treatment of cancer. There is not sufficient space in the protocol to discuss the complete aspects of glucose modulation therapy, but this is described in detail in Dr. Quillin's book, Beating Cancer with Nutrition. You can order it directly from the publisher by calling (918) 495- 1137. (The cover price is $14.95.)

The Foundation's Adjuvant Cancer Treatment Protocol

The Foundation's Adjuvant Cancer Treatment Protocol is for most forms of cancer. This protocol assumes that the patient's primary tumor has been eradicated, at least partially, by surgery or by some other treatment. However, it may be followed even if the primary tumor has not yet been eradicated. The following is a step-by-step treatment plan.

Step One- Arrange for monthly blood tests, including

Tumor marker tests. The type of cancer dictates the type of test used. Some cancers do not have a specific tumor marker test available.
Immune cell subset test. (This is an expensive test.)
Complete blood chemistry. To include all standard liver, thyroid, heart, and kidney function tests. (This is a low-cost test.)

These blood tests must be taken on a regular basis under the supervision of a physician in order to follow scientifically the Foundation's Cancer Treatment Protocol. It's the best way of knowing whether what you are taking is working and/or whether significant toxicity is developing. This is no time to guess! Since you will be having these tests performed monthly, you should price-shop for the best deal. The Life Extension Foundation offers these tests at discount prices, but if you have health insurance, it would save you money in the long run to have these tests performed by your physician.

Here are some accepted blood tumor markers for common cancers:

Type of Cancer	Tumor Marker Blood Test
Ovarian cancer	CA 125
Prostate cancer	PSA and prolactin
Breast cancer	CA 27.29, CEA, alkaline phosphatase and prolactin (some doctors use the CA 15-3 in place of the CA 27.29)
Colon, rectum, liver, stomach and other organ cancers	CEA, GGTP
Pancreatic cancer	CA 19.9, CEA, GGTP
Leukemia, lymphoma, and Hodgkin's disease	CBC with differential, immune cell differentiation and leukemia profile
Lung cancer	CEA, CA 125, alkaline phosphatase PT, PTT and D-Dimer of fibrin

Step Two: Total nutritional support:

Life Extension Mix (high-potency multinutrient supplement): the standard daily dose involves 3 tablets, 3 times a day. It is also available in powder or capsule form to be taken in 3 divided doses.
Life Extension Herbal Mix-powder only. Take 1 tablespoon early in the day.
Super Selenium Complex: take 1 tablet, 2 times a day.
Green Tea capsules (decaffeinated): take 4 to 10 capsules a day in divided doses.
Coenzyme Q10 (oil-filled capsules): take 200 to 400 mg early in the morning.
Garlic-Kyolic Garlic Formula 105: take 4 capsules a day; and PureGar (high allicin garlic): take four 900-mg capsules a day with meals.
Essential fatty acids. Mega EPA fish oil or Udo's Choice Ultimate Oil: take the highest tolerable dose. The suggested dose is 8 to 12 Mega EPA caps along with 4 MEGA GLA capsules to balance the high amount of omega-3 being consumed in the fish oil. (Some studies suggest not taking these oils if you have prostate cancer.)
Vitamin C capsules or powder: take the highest tolerable dose (4000 to 12,000 mg) of pharmaceutical grade vitamin C (to be taken throughout the day).
Phyto-Food powder: take 1 to 2 tablespoons daily. Juicing organic vegetables is an alternative to Phyto-Food powder.
Curcumin: take four 500-mg capsules daily.
Conjugated linoleic acid (CLA): Take four 1000-mg capsules in two divided doses.

Step Three: Boosting immune function:

If the immune system is weakened enough, cancer cells can survive and multiply. The most critical part of the immune system is the thymus gland, a small organ just below the breast bone that governs the entire system. There are several products that promote healthy thymic activity.

Thymex is a product used by alternative physicians to stimulate immune function. It provides extracts of fresh, healthy tissue from the thymus and other glands that produce the disease-fighting cells of our immune system. The primary ingredient in Thymex is immunologic tissue from the thymus gland. Also included in Thymex is tissue from the lymph nodes and spleen that produces the white blood cells that engage in life-or-death combat with invading organisms in our bloodstream under the "instruction" of the thymus gland. Thymex is a synergistic formula that contains herbal activators and a full complement of natural homeopathic nutrients, in addition to fresh, healthy thymus, lymph, and spleen tissues. Thymex is a professional formula normally dispensed through doctor's offices. Thymex has been used extensively to amplify the immune potentiating effect of DHEA replacement therapy. According to a physician most familiar with DHEA, thymus extract is required to obtain the immune system-boosting benefit of DHEA.

KH3. Cancer patients usually have elevated cortisol levels that can suppress immune function. Take 1 to 2 tablets of KH3 daily on an empty stomach first thing in the morning and 1 or 2 KH3 tablets in the mid-afternoon on an empty stomach to suppress the damaging effects of cortisol.

DHEA can also suppress dangerously high cortisol levels while boosting immune function via other mechanisms. Doctors usually prescribe at least 25 mg per day of DHEA for their male cancer patients and a minimum of 15 mg a day of DHEA for females. Your monthly or bimonthly DHEA-S and immune cell subset tests and tumor marker tests will determine whether DHEA is producing a beneficial effect. Do not use DHEA if you have prostate cancer or estrogen-sensitive breast cancer.

Melatonin boosts immune function via several mechanisms of action. It also exerts an inhibitory effect on cancer cell proliferation and induces the differentiation of cancer cells into normal cells. Melatonin should be taken every night in doses ranging from 3 to 40 mg.

CAUTION: Some doctors are under the impression that leukemia, Hodgkin's disease, and lymphoma patients should avoid melatonin until more is known about its effects on these forms of cancer. If melatonin is tried in these types of cancer, tumor blood markers should be watched closely for any sign that melatonin is promoting tumor growth.

Show your oncologist the information in this book regarding the use of the FDA-approved drugs interleukin-2 or interferon and melatonin. Studies document that low doses of interleukin-2 or alpha-interferon combined with high doses of melatonin (10 to 50 mg nightly) are effective against advanced, normally untreatable cancers. Ask your doctor to prescribe these agents:

Interleukin-2 at a dose of 3 million units injected subcutaneously six out of every seven days for 6 weeks.
(One month later) Alpha-interferon at a dose of 100,000 to 300,000 units injected subcutaneously six out of seven days for six weeks. Subcutaneous injections can be self-administered at home.

This immune-boosting program should be adjusted if the immune cell subset test or tumor marker tests fail to show marked improvement in the patient's immune function. For example, if there are too many T-suppressor cells, 800 mg a day of the drug Tagamet (now available over the counter) can lower the T-suppressor cell activity. T-suppressor cells often are elevated in cancer patients, which prevents them from mounting a strong immune response to the cancer.

Step Four: Inhibiting cancer cell proliferation:

Water-soluble vitamin-A liquid in doses of 100,000 to 300,000 IU a day should be used for several months. In lieu of high-dose vitamin A supplementation, it would be better to have a physician prescribe a vitamin A analog drug such as Accutane.

CAUTION: Monthly blood tests can help ascertain whether toxicity is occurring in response to these high doses of vitamin A. Do not take vitamin A if you have thyroid cancer or suffer severe thyroid deficiency. (Refer to the Avoiding Vitamin A Toxicity protocol)

Melatonin (taken to boost immune function) also inhibits cancer cell proliferation.
Mega Soy Extract: take five 700-mg capsules 4 times a day. Soy may be effective in treating certain cancers. Genistein is the most substantiated soy isoflavone that produces multiple cancer-inhibiting effects. Genistein has been shown to work especially well against certain leukemias and cancers of the skin, prostate, and brain.

CAUTION: For most cancers, the determining factor of whether soy may work is whether your cancer cells carry a mutated p53 tumor suppressor gene, or whether they carry functional p53. If functional p53 is present, then soy genistein will probably not work. In small-cell lung cancer, however, it was recently determined that genistein's growth-inhibiting effects were independent of p53 function. Only specialized tumor cell tests (immunohistochemistry) can determine the p53 status of your particular cancer. Estrogen-receptor-positive breast cancer patients should avoid high doses of genistein.

Take whey protein concentrate powder, 30 to 60 grams a day (1 to 2 scoops). Whey protein concentrate inhibits cancer cell glutathione levels, making cancer cells more vulnerable to free-radical destruction than normal cells.

Step Five- Inducing cancer cell differentiation.

Cancer cells are aberrant, transformed cells that proliferate (divide) more rapidly than normal cells until they kill the patient. Inducing cancer cells to "differenti