~Cancer Adjuvant Therapy, Part 3

COMPLEMENTARY THERAPIES, continued

Green Tea

Salicylic acid, the main anti-inflammatory component of aspirin, is a naturally occurring compound found in green tea, having COX-2 inhibiting qualities. The polyphenols and flavonoids contained in green tea are also COX-2 inhibitors (Noreen et al. 1998).

Mayo Clinic researchers showed that green tea consumption inhibited cancer growth (Paschka et al. 1998). They identified the green tea polyphenol EGCG (epigallocatechin gallate) as the most potent inhibitor of cancer cell proliferation. Japanese researchers pinpointed the types of cancer most responsive to green tea (breast, esophageal, liver, lung, skin, and stomach) by surveying cancer-free individuals who consumed 4-6 cups of green tea a day.

The odds ratio of stomach cancer decreased to 0.69 with a high intake of green tea (7 cups or more a day) (Inoue et al. 1998). Another study conducted in Yangzhong (a region in China with a high incidence of chronic gastritis and gastric cancer) showed the amount and duration of green tea consumption governed the rate of stomach cancer. Frequent long-term green tea drinkers had approximately 50% less risk of developing gastric cancer compared to individuals consuming little or no tea (Setiawan et al. 2001). Green tea reduces the damaging effects of nitrites in the acidic environment of the stomach with greater efficiency than vitamin C.

The growth of non-Hodgkin's lymphoma cells, transplanted in mice, was reduced by 50% when green tea was a part of the animal's diet. Cyclophosphamide, a chemotherapeutic drug, administered at the maximum tolerable dose, was unable to replicate similar benefits (Bertolini et al. 2000). Part of green tea's anticancer profile includes an antimutagenic factor that helps DNA replicate accurately (Uhlenbruck et al. 1998).

PGE2 is thought to stimulate tumor promotion in precancerous and cancerous cells (August et al. 1999; Bertolini et al. 2000). Of 14 subjects, 10 (71%) demonstrated a response to green tea, as evidenced by at least a 50% inhibition of PGE2 in rectal mucosa.

EGCG appears to normalize the cell growth cycle and prompt apoptosis in cancer cells by inhibiting NF-kB, a growth vehicle cancer cells use to escape cell regulatory control (Ahmad et al. 2000). EGCG strongly and directly inhibits telomerase, an enzyme (normally dormant from birth) that delivers immortal status to cancer cells (Naasani et al. 1998).

Cigarette smokers who drink green tea have a 45% lower risk of lung cancer compared to non-tea drinkers. Even though Japan has one of the highest numbers of smokers in the world, they have one of the lowest rates of lung cancer of any developed nation, a protection thought to be delivered by green tea.

The number of anticarcinogens, antioxidants, and anti-proliferative agents found in green tea (carotenoids, chlorophyll, polysaccharides, vitamins C and E, and numerous flavonoids) explains why some researchers advocate using a broad-spectrum extract, replicating the plant's total constituents. Considering the vastness of green tea’s anti-cancer effects, incorporating green tea into the diet 5-10 cups a day (or five 350-mg capsules three times a day of a 95% polyphenol extract) would appear to be wise for individuals concerned with cancer.

Curcumin

Worldwide clinical trials have chiseled out a definite place for curcumin in oncology. Among them are New York Presbyterian Hospital and the Weill Medical College, which reported that curcumin, a curcuminoid found in turmeric, directly inhibited the COX-2 enzyme (Zhang et al. 1999). So excited are various oncologists regarding curcumin that the potent anti-inflammatory has been classed as a potential third generation cancer chemopreventive agent.

Curcumin inhibited thromboxane A2 (TxA2), a highly unstable, biologically active compound created by COX from AA (Shah et al. 1999; Newmark et al. 2000). Unless controlled, TxA2 promotes tumor endothelial cell migration (metastasis) and angiogenesis. By inhibiting TxA2, curcumin reduces the tumor's blood supply and lessens the threat of metastasis (Arbiser et al. 1998; Nie et al. 2000). Curcumin is effective at inhibiting 5-lipoxygenase and subsequently HETE, a survival factor for prostate, breast, and pancreatic cancers (Ghosh et al. 1998; Ding et al. 1999; Newmark et al. 2000; Li et al. 2001).

The following list illustrates the depth of curcumin's defenses against cancer:

  • Colon: Curcumin inhibited chemically induced carcinogenesis in the colon when administered at different stages of the cancer process. Laboratory rats, administered curcumin during either initiation or late in the premalignant phase, had a lesser incidence and fewer numbers of invasive malignant colon tumors (Kawamori et al. 1999). Also, by inhibiting COX-2-arachidonic acid interactions, curcumin suppresses prostaglandins responsible for inflammatory processes (Plummer et al. 1999). Chronic inflammation has for decades been regarded as a cause of colon cancer (Konig et al. 1976).

  • Antioxidant activity: Curcumin inhibits or possibly even reverses oxidative damage by scavenging and neutralizing free radicals. By defusing the hydroxyl and superoxide radicals and breaking oxidative chain reactions, curcumin protects DNA with greater efficiency than lipoic acid, vitamin E, or beta-carotene (Ruby et al. 1995; Ahsan et al. 1999; Li et al. 2001).

  • Breast cancer: Curcumin inhibits the growth of multiple breast cancer cell lines (Inano et al. 1999), particularly those that result from exposure to environmental estrogens such as chemicals and pesticides (Verma et al. 1998). Also, curcumin, estrogen, and estrogen mimickers gain entry into the cell through the aryl hydrocarbon receptor. Because curcumin competes for entry, it can crowd out damaging materials (Ciolino et al. 1998). According to researchers, curcumin blends well with other cancer inhibitors. For example, a curcumin-isoflavonoid combination suppressed the growth of estrogen receptor-positive cancer cells up to 95% (Verma et al. 1998).

  • Oral tumors: Curcumin inhibits oral squamous cell carcinoma more effectively than either genistein or quercetin (Ellatar et al. 2000). Only cisplatin, a platinum-based chemotherapy drug, was more effective.

  • Skin tumors: Curcumin inhibits skin tumors. When applied topically, curcumin reduces skin inflammation and inhibits local swelling (Huang et al. 1997).

  • Prostate cancer: Curcumin was able to decrease the proliferative potential of androgen-independent prostate cancer cells--and cells of other androgen-dependent cancers--largely by encouraging apoptosis. Moreover, a significant decrease in microvessel density, the sustaining blood supply of a tumor, was also observed (Dorai et al. 2001).
  • Leukemia: Curcumin-induced apoptotic cell death in promyelocytic leukemia HL-60 cells at concentrations as low as 3.5 mcg/mL (Kuo et al. 1996).

  • Protein kinase C (PKC) and epidermal growth factors (EGF): Curcumin was proclaimed "potentially useful" in developing anti-proliferative strategies to control tumor growth by suppressing the activity of protein kinase C (PKC) (Korutla et al. 1995). As the activity of PKC is slowed down, tumor proliferation is halted (Lin et al. 1997). PKC transmits signals from the epidermal growth factor receptor (EGF-R), a cycle that ultimately encourages the growth of tumors. Conversely, cancers awaiting EGF stimulation are dealt a severe blow if this pathway is severed. Curcumin blocked the activation of EGF by 90%.

  • p53 potentiator: Curcumin increases expression of healthy nuclear p53 protein in human basal cell carcinomas, hepatomas, and leukemia cell lines (Jee et al. 1998). Turn to the protocol Cancer: Gene Therapies, Stem Cells, Telomeres, and Cytokines to read more about tumor suppressor genes.

  • Tumor necrosis factor-alpha (TNF-alpha): Researchers at the University of Kentucky showed that TNF-alpha acts as a catalyst in cytokine production, stimulating interleukin-6 (IL-6) and -8 (IL-8) and activating NF-kB (Blanchard et al. 2001). Curcumin inhibits TNF-alpha, thus blocking TNF-alpha, NF-kB pathways, and the emergence of pro-inflammatory cytokines (Xu et al. 1997-1998; Li et al. 2001; Literat et al. 2001). To read more about proinflammatory cytokines, turn to the protocol Cancer: Gene Therapies, Stem Cells, Telomeres and Cytokines.

  • Helicobactor pylori: Exposure of gastric epithelial cells to the ulcer-causing bacterium H. pylori (considered a potential gastric and pancreatic carcinogen) induces secretion of IL-8. IL-8 plays a pivotal role in the development of cancer. The more virulent H. pylori, the greater the production of IL-8. H. pylori strains that fail to induce IL-8 secretion do not activate NF-kB, while all IL-8 inducing strains activate the transcription factor. Curcumin is capable of inhibiting NF-kB and completely suppressing IL-8. By restraining essential players in the development of H. pylori, curcumin diminishes the risks of both gastric and pancreatic cancer (Munzenmaier et al. 1997; Stolzenberg-Solomon et al. 2001).


Although the benefits of curcumin are impressive, curcumin is poorly assimilated. This means that while the digestive tract and liver profit, the remainder of the body may be denied benefit. Administering 2000 mg of curcumin showed that very little reached the bloodstream. This dilemma is amendable by adding a small amount of piperine (a component of black pepper) to curcumin, increasing bioavailability by 2000% (Shoba et al. 1998). However, it is possible that piperine in combination with prescription drugs could increase the bioavailability of the drug. Therefore, it is recommended that curcumin (containing piperine) be taken 2 hours apart from prescription medications.

Super Curcumin dosage: Healthy people typically take 900 mg of curcumin each day. Cancer patients often take as much as four 900-mg capsules 3 times a day for a 6- to 12-month period, reducing the dosage thereafter. Individuals with biliary tract obstruction should avoid curcumin because it enhances biliary flow from the liver. High doses of curcumin should not be taken on an empty stomach to protect against gastric irritation.

Note: The question ultimately arises as to whether curcumin is appropriate during chemotherapy. A recent study from the University of North Carolina (Chapel Hill) showed that curcumin reduced the effectiveness of chemotherapy in breast cancer patients by inhibiting reactive oxygen species (Somasundaram et al. 2002). Please refer to the protocols Cancer: Should Patients Take Dietary Supplements? and Cancer Chemotherapy to read more about this study and the advisability of taking curcumin during conventional treatment.

Dimethyl Sulfoxide (DMSO)

In August 1995, Dr. Julian Whitaker, M.D., relayed his own experience with DMSO, when a basal cell carcinoma (about the size of a dime) appeared on his ear. A dermatologist recommended surgical removal of the cancerous portion and a skin graft replacement. Instead, Dr. Whitaker made a paste from shark cartilage, vitamin C, and DMSO and applied the mixture to the lesion daily. Within 3.5 weeks, the basal cell had completely disappeared. Stanley Jacob, M.D., professor at the Oregon Health Sciences University (Portland) suspected DMSO was the hero, although Dr. Whitaker has confidence in the full formula (Whitaker 1995).

The Sealy Center for Molecular Sciences reported that DMSO, administered either before or 15 minutes after TNF-alpha, blocked 80% of NF-kB. By suppressing TNF-alpha and NF-kB, DMSO broke an inflammatory cascade that otherwise terminates in an onslaught of potentially damaging cytokines (Vlahopoulos et al. 1999).

DMSO is an excellent transporter of other therapies into cancerous cells. In fact, many offshore cancer clinics consider it the standard for all patients who are undergoing various therapies.

Essential Fatty Acids (EFAs)--block arachidonic acid, inhibit COX-2 enzyme, regulate cell division and inhibit adhesion, prevent cachexia, potentiate traditional cancer therapies, and suppress the activity of pro-inflammatory cytokines

As a result of the current fat phobia, over 80% of Americans consume inadequate amounts of essential fatty acids (especially omega-3 fatty acids). Physicians report that this scarcity is contributing to epidemic proportions of degenerative diseases, including cancer (Murray et al. 1996). The omega-6 to omega-3 fatty acid ratio typically seen may be as high as 20:1, whereas the optimal ratio may be nearer 1:1 (Mercola 2002a). EFAs, although not manufactured by the body, perform vital functions that prevent and control cancer.

  • As enzymes metabolize AA, the byproducts of the metabolism fuel the cancer process (Comprehensive Cancer Care 2001). Oxidized AA is, in fact, considered a primary initiator of cancer (Newmark et al. 2000). One gram of omega-3 fatty acids blocks 10 grams of AA (Pizzorno 2001).

  • The COX-2 enzyme (interacting with AA) can cause excess production of PGE2, promoting cancer cell growth. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (derived from alpha-linolenic acid or fish oil) are effective COX-2 inhibitors (Ringbom et al. 2001).

  • Fish oil is the most documented supplement to suppress (up to 90%) a cascade of damaging cytokines, including TNF-alpha and IL-1 (James et al. 2000). It should be noted that psychological stress induces the production of pro-inflammatory cytokines, such as TNF-alpha, IL-6, and IL-10. Increasing omega-3 fatty acids lessened the pro-inflammatory response to psychological stress (Maes et al. 2000). For information regarding a blood test to obtain a cytokine profile, call (800) 208-3444.

  • Women with high levels of alpha-linolenic acid in breast tissue have a 60% lower risk of breast cancer compared to women with low levels (Klein et al. 2000; Maillard et al. 2002). Jeffrey Bland, esteemed scientist and teacher, reported a supportive study involving 500 (C3H) mice prone to breast cancer. The mice were divided into 10 groups of 50 animals and evaluated regarding the impact of various dietary oils on the occurrence of cancer. One-tenth of the animals received standard chow and served as a control group; another group received standard chow plus benzanthracene, a carcinogen. The other eight groups received isocaloric diets along with the cancer inducer; the variable was the type of fat (not the amount) fed in conjunction with the chow. Eight oils were evaluated: tallow, fish, corn, primrose, safflower, linseed oils, and two others. At the conclusion of the study, eight of the 10 groups (400 animals) were dead with mammary cancer. The 100 survivors were animals fed omega-3 rich oils. The study was repeated using different types of oils and varying amounts of the cancer inducer. The end results werethe same. Researchers postulated that the advantage of omega-3 fatty acid was the oil's ability to reduce inflammatory mediators, those signaling tumor progression and metastasis (Cameron et al. 1989).

  • Epidemiologic and experimental studies suggest that oils rich in omega-3 fatty acids lessen the risk of colon cancer. A relatively small fraction of alpha-linolenic-rich perilla oil (25% of total dietary fat) provided an appreciable beneficial effect in reducing cancer risk (Narisawa et al. 1994).

  • Low EFA status results in a lack of oncogene control with a shift toward cell proliferation (Pizzorno 2001). EFAs also regulate the adhesiveness of cancer cells, including cell-cell and cell-matrix adhesions (Jiang 1998).

  • Fatty acids, particularly EPA, inhibited the growth of three human pancreatic cancer cell lines (MIA PaCA-2, PANC-1, and CFPAC), suggesting therapeutic benefit to pancreatic cancer patients (Falconer et al. 1994).

  • Omega-3 fatty acids prevent cachexia (the muscle wasting and weight loss that occurs in some cancer patients irrespective of proper nutritional intake). Controlling the symptoms common to cachexia (anorexia, abnormal macronutrient metabolism, and fatigue) improves quality of life and extends periods of remission (Bruera 2003).

  • Researchers found DHA and EPA cytotoxic to myeloma cells in vitro (Sravan et al. 1997). Individuals who regularly consume fish and cruciferous vegetables appear to lessen their risk of developing multiple myeloma (Brown et al. 2001).


Thirty-two dogs with Stage III lymphoma and their response to a dietary and chemotherapeutic regime were evaluated. All of the animals were fed identical diets, but they received varying types of oils. For example, one group received menhaden fish oil (rich in omega-3 fatty acid) and arginine, while the control group received soybean oil (Ogilvie et al. 2000). The animals also received doxorubicin every 3 weeks.

As DHA and EPA levels increased in the test group, the animals experienced longer disease-free intervals and subsequently increased survival time. Dogs receiving the supplemented diet lived about 700 days; animals receiving the soybean oil lived only about 400 days. The time until relapse was also significant: 425 days in the treatment group versus 275 days in the control group. Note: Since fish oil increases the effectiveness of chemotherapeutic agents, the animals receiving the menhaden oil realized an additional advantage over the soybean-treated animals (Hardman et al. 2001).

Suggested dosages for various EFAs: Take six 1000-mg capsules a day of perilla oil, which provide 550-620 mg of alpha-linolenic. Flaxseed oil, 1000-mg softgels, is a rich source of omega-3 fatty acids. Take 7 softgels a day. A preventive dose of a fish oil concentrate called Mega EPA is 4 capsules a day (2800 mg of EPA/DHA). Cancer patients often use 8-12 Mega EPA softgels daily along with 4 Mega GLA softgels to balance the high amount of omega-3 being consumed in the fish oil. Another option for cancer patients is 8 capsules a day of Super GLA/DHA, providing a highly concentrated amount of DHA, GLA, and a moderate amount of EPA. Higher dosages should be physician supervised.

Garlic (Allium sativum)--is inhibitory to a number of malignancies, minimizes damage imposed by known carcinogens, and boosts the immune system No plant has the medicinal history, spanning as many cultures, of garlic. Garlic, in fact, appears to be the quintessential medicine/food, having influence on simplistic diseases from common colds to degenerative diseases. For centuries the Chinese have used garlic-containing herbal formulas to treat tumors, but scientists were challenged to find the mechanism that rendered it efficacious.

Among those dedicated to validating garlic is Dr. Benjamin Lau, M.D., Ph.D. Dr. Lau, focusing upon cancer biology and immunology, was motivated by an epidemiological study reported by the People's Republic of China. The study compared two large populations in the Shandong Province: Cangshan Country and Qixia Country (Mei et al. 1982). Residents of Cangshan County experienced the lowest death rate due to stomach cancer (three per 100,000), regularly consuming about 20 grams of garlic a day; the people of Qixia had a 13-fold higher stomach cancer death rate, eating garlic only rarely. It appears that lowering nitrite concentrations may be the protective mechanism resulting in fewer numbers of gastric cancers. Jhinzou Liu, Ph.D., a Chinese biochemist, found garlic "much more effective than vitamin C" in keeping nitrosamines, potentially carcinogenic compounds, from forming.

Garlic's anticarcinogenic effects are not restricted to gastric malignances.

  • Garlic (administered intralesionally to mice) was significantly more effective than BCG (bacillus Calmette-Guerin), a weakened form of the tuberculosis bacilli, in treating bladder cancer (Lau et al. 1986).

  • Garlic extract reduced the incidence of breast cancer (in mice) by 70-90% (Langer 1991).

  • Diallyl disulfide, a sulfur compound, induced cell death (apoptosis) in non small cell lung cancer cells (Hong et al. 2000); Diallyl sulfide, a component of garlic oil, inhibited liver carcinogenicity following carcinogenic exposure (Hayes et al. 1987); S-allyl cysteine, (a derivative of aged garlic extract), inhibited human neuroblastoma cell growth in vitro (Welch et al. 1992); allixin, one of the compounds of aged garlic extract, inhibited the development of skin cancer (Nishino et al. 1990). Diallyl sulfide was highly inhibitory during the initiation phase of esophageal cancer (Wargovich et al. 1992).

  • S-allyl cysteine (SAC) inhibited proliferation and cell growth of nine human and murine melanoma cell lines, producing positive results without side effects (Takeyama et al. 1993). Of equal importance, garlic modulated major cell differentiation markers of melanoma. As the cell shows distinguishable characteristics (differentiation), it eventually loses its uncontrollable propensity to divide.

  • S-allyl cysteine and diallyl sulfide reduced colonic damage and the incidence and frequency of colon tumors if administered 3 hours prior to each carcinogenic injection. Colonic damage was inhibited by 36% and 47% respectively (Sumiyoshi et al. 1990). Michael Wargovish, M.D. (Houston), claims that diallyl sulfide is one of the most active chemopreventive agents known.


S-allyl cysteine (SAC) appears to be able to overcome the adverse side effects (heart and liver damage) associated with the chemotherapeutic agent doxorubicin. Doxorubicin resulted in a 58% mortality rate among laboratory mice; SAC reduced doxorubicin-induced mortality to 30% (Mostafa et al. 2000). Weight loss, typical with doxorubicin, was reduced from 13% to 9% with SAC.

Certain garlic constituents possess antioxidant properties, while other constituents act as oxidants. The latter case is strikingly demonstrated when human hemoglobin is mixed with extracts from fresh garlic and from dried raw garlic powder products. The hemoglobin-garlic extract mixtures turn dark, and their spectra reveal the oxidation of hemoglobin to methemoglobin. Contrarily, extracts from aged garlic do not cause oxidative changes.

When t-butylhydroperoxide, a free-radical generator and oxidant, is used to oxidize red blood cells, it results in rupturing of the cells and darkening of the hemoglobin. An extract of aged garlic, added to the red blood cell suspension prior to the addition of the oxidant, minimized oxidation and cell rupture (Lin 1989). Since many cancer therapies produce free radicals in an attempt to kill cancer cells, researchers concluded that garlic could offer significant protection against treatment-induced tissue damage. Comment: Please consult the protocol Cancer: Should Patients Take Dietary Supplements to read about the appropriateness of antioxidant therapy during conventional cancer treatment.

Another benefit of garlic to the cancer patients is its effect on enhancing immune function. Here are a few of the numerous studies relating to garlic's effect on immune cells:

  • Garlic stimulates proliferation of lymphocytes, those cells comprising 25% of total white blood cells that carry out the principal responsibilities of the immune system (Colic et al. 2000).

  • Garlic quickens macrophage phagocytosis, a process by which microorganisms and cellular debris are engulfed and destroyed (Lau et al. 1991).

  • Fraction 4 (F4), a protein isolated from aged garlic extract, enhanced the cytotoxicity of human lymphocytes. Although F4 alone increased cytotoxicity, the effect was amplified when F4 was combined with suboptimal doses of interleukin-2. F4 is an efficient immune potentiator and may be used for immune therapy (Morioka et al. 1993).


T-helper/T-suppressor ratios converted to normal among a small group of AIDS patients supplementing with garlic. Thrombocytopenia (a reduction in platelet count) is often therapy-resistant in individuals with AIDS. Yet, platelet numbers have been reported to increase, sometimes greater than 100,000, during 4 months of garlic supplementation. Although AIDS is not cancer, this feared disease has forced researchers and clinicians to look closely at the immune system (Abdullah et al. 1989).

Research suggests that garlic preparations are not equal in pharmacologic value. While raw garlic juice, heated garlic juice, dehydrated garlic powder, and aged garlic extract all significantly enhanced natural killer cell numbers and activity, only aged garlic extract and heated garlic juice inhibited the growth of tumor cells in mice (Kasuga et al. 2001).

Dr. Abdullah evaluated the percentage of tumor kill using raw and aged (Kyolic brand) garlic. Raw garlic killed 139% of tumor cells compared to an untreated group, while Kyolic killed 159% (Abdullah et al. 1988). Note: Defining the most efficacious type of garlic is confounding. Some physicians and clinicians report greater gains from odorous garlic supplementation. If garlic is part of your nutritional program, experiment with different varieties, assessing both subjective and objective improvements. It is highly possible that different metabolic types respond differently to various forms of garlic.

A good source of supplemental garlic is PureGar Caps. PureGar Caps contain the highest available potency (9 mg) of the active allicin compound, deemed by some as the yardstick for measuring the worth of garlic. Use 4 capsules, 2-4 times daily, with meals. If Kyolic aged garlic is the selection, use one 1000-mg caplet daily with meals. PureGar can cause a temporary gastric burning and pungent odor, whereas Kyolic aged garlic extract is free of these effects. No serious side effects have been reported.

Evaluating hundreds of garlic users, however, it should be noted that garlic thins the blood, and for some individuals (particularly those using anticoagulants) it is essential to abstain from or to watchfully monitor supplementation coagulation status.

Therapeutic factors contained in garlic include magnesium, selenium, 17 amino acids, 33 sulfur compounds, and vitamins B1, A, and C, as well as germanium. Germanium has been shown to induce production of interferon, enhance natural killer cell activity, and activate macrophage activity in experimental animals (Aso 1985).

Glutamine--increases NK cell activity, decreases PGE2 synthesis, inhibits tumor growth, stabilizes weight loss, and reduces incidence of stomatitis and infection

Tumors typically have high concentrations of glutamine; thus, physicians have been reluctant to add supplemental glutamine to a cancer protocol. However, oral glutamine (1 gram per kg of body weight a day administered to rats) upregulated tissue glutathione (a powerful antioxidant) by 25% and increased natural killer cell activity 2.5-fold. PGE2 synthesis (a pro-inflammatory prostaglandin that fuels tumor growth) decreased and tumors were inhibited by 40% (Klimberg et al. 1996a).

When glutamine accompanied either chemotherapy or radiotherapy, it protected the host and actually increased the selectivity of therapy for the tumor. This was evidenced among a group of rats (receiving either methotrexate, cyclophosphamide, or cisplatin) whose tumor reduction nearly doubled with glutamine supplementation (Klimberg et al. 1992, 1996b).

Researchers also observed that glutamine decreased progression of tumor formation in rats implanted with mammary tumors, suggesting oral glutamine may be useful as a chemopreventive in breast cancer (Feng et al. 1997). Oral glutamine maintained lymphocyte numbers and protected the gut of esophageal cancer patients during radio/chemotherapies (Yoshida et al. 1998).

Glutamine typically stabilizes weight loss by preserving intestinal function and allowing better nutrient absorption. Subsequently, glutamine prolongs survival by slowing down catabolicwasting, a disorder characterized by weight loss, diminished muscle mass, and loss of body fat. Fewer incidences of stomatitis (a generalized inflammation of the oral mucosa) and bouts of infection help reduce the number of days spent in a hospital (Anderson et al. 1998). Harvard University research showed that glutamine supplementation decreased medical expenses of leukemia patients undergoing bone marrow transplants by $21,095 per patient (MacBurney et al. 1994). (The retail cost of glutamine is $10.00 per day.)

A suggested glutamine dosage is 2 or more grams a day taken on an empty stomach. Glutamine is regarded as nontoxic, but cancer patients contemplating higher dosages should do so only after consulting with a health care provider.

Continued . . .


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