For The Technically-Oriented Reader

This chapter is provided for the person who enjoys knowing more of the intimate details on how nutrition interrupts the cancer process. This section is to be considered more exemplary rather than comprehensive. If I included all the data in this field, then this book would be unwieldy. These references provide a scientific foothold upon which to recommend nutrition therapy in conjunction with traditional oncology care. For more information, see:

Non-Technical CANCER THERAPY, by Ralph Moss, PhD CANCER AND ITS NUTRITIONAL THERAPIES, by Richard Passwater, PhD BEATING THE ODDS, by Albert Marchetti, MD WHAT YOUR DOCTOR WON’T TELL YOU, by Jane Heimlich VITAMINS AGAINST CANCER, by Kedar Prasad, PhD HOW TO FIGHT CANCER AND WIN, by William Fischer


Purpose of Using Adjuvant
Nutrition in Cancer Treatment

1. Preventing malnutrition. Cancer is a serious wasting disease, elevating basal metabolism, altering bio-energetics, and oftentimes inducing anorexia. The net effect is that 40% or more of cancer patients actually die from malnutrition, not from the cancer.1 The American College of Physicians issued a position paper in 1989 stating:”…the evidence suggests that parenteral nutritional support [in cancer treatment] was associated with net harm, and no conditions could be defined in which such treatment appeared to be of benefit.”2 This “meta-analysis” of the literature specifically excluded cancer patients who were malnourished. Nutrition support is meant to relieve malnutrition, not cure cancer. Extensive chemotherapy or radiation therapy are, in themselves, sufficient stressors to induce catabolic malnutrition.3 Additionally, standard Intensive Care Unit parenteral formulas may be inappropriate for cancer patients since high glucose solutions may feed tumor growth.

2. Bolstering immune functions. From textbooks4 to extensive reviews of the literature5, it has been clearly demonstrated that a strong link exists between nutrient intake and the quality and quantity of human immune factors. Researchers provided 30 milligrams of beta carotene (or 50,000 iu, which is 10 times the Recommended Dietary Allowance of vitamin A), to healthy older adult volunteers with a dose dependent increase in natural killer cell activity (NK) and interleukin-2 receptors.6 Similar results have been found with vitamin E, B-6, C, and zinc.

3. Nutrients as biological response modifiers.

Immune modulation

cleave immune complexes: i.e. proteolytic enzymes

improve quantity: via precursors for immune cytotoxic activity, nitric oxide from arginine for enhanced chemotaxis; increase NK, TNF, total lymphocytes via beta carotene, vitamin A, C, E, B-6 etc.

improve quality: via increase in tumor recognition using enzymes or emulsified vitamin A

reduce antigens: via oligoantigenic diet

thymotropic: via arginine supplements and thymus gland extract

immune sparing: antioxidants that lower turnover in cell mediated immunity or an increase in circulation of immune factors, i.e. vitamin E protects lymphocytes from oxidative damage in chemotaxis

Alter genetic expression

down regulate oncogene: i.e. soybean protease inhibitors alter c-myc oncogene

genetic repair: increase DNA polymerase activity and decrease in base pair fragility via zinc & folate

inhibit episome production: via vitamin D

directly affect gene receptors: i.e. vit. A

Alter cell membrane dynamics

K to Na ratio: may alter membrane permeability & thus flow of oxygen & nutrients into & out of cell (an anaerobic environment is more conducive to tumor cell mitosis)

dietary fat intake: affects lipid bi-layer content in cell membrane, thus membrane dynamics & oxygenation

prostaglandin metabolism: macronutrients influence hormones which influence prostaglandin branch points, which can affect aggregation and adhesiveness of cell membranes, thus metastatic potential of tumor

Influence detoxification

urinary output: fluid intake & diuretics (e.g. coffee & alcohol)

fecal excretion: fluid and fiber intake coupled with nutrients that encourage peristalsis

cytochrome P450

endogenous biosynthesis of detoxification enzymes: catalase, SOD, GSH through selenium and vitamin E

immune stimulation: encourages detox

low temperature saunas encourage excretion of toxins via skin pores

respiratory quotient indicates efficiency of oxidative respiration, which can be retarded by heavy metal toxicity

Alter acid/base balance

all foods influence pH. Tumor cells thrive in acidosis.

alkalizing diet (high in most plant food items) encourages detox of heavy metals

Cell/cell communication

gap cell junctions for ionic communication between cells and nucleus, i.e. vitamin A may be able to revert abnormal DNA back to normal DNA (prodifferentiation or cytodifferentiation) and cell content via gap cell junction

Prostaglandin synthesis

affected by macronutrient intake and serum insulin levels

immune modulation: PGE-1 vs PGE-2, via eicosapentaenoic acid or gamma linolenic acid

membrane aggregability and metastasis are heavily influenced by prostaglandin metabolism

estrogen binders: PGE-1 increases endogenous biosynthesis of circulating estrogen receptors, PGE-1 probably also helps with androgen-driven prostatic cancer

Affect steroid hormone activity

fat from diet and body influence estrogen output

phytoestrogens in diet (i.e. soybeans): may retard hormone-driven cancer lignans (from plant food) can provide estrogen binders or analogs to educe estrogen activation of tumors

Alter polyamine synthesis

polyamines can accelerate cancer growth, while B-6 creates polyamine complexes and accelerates their excretion


selective starve tumors by:

depriving anaerobic and fermenting tumors of their preferential substrate, glucose

altering mitochondrial membranes of tumor, such as with Vitamin C

employ nutrients that encourage aerobic metabolism: CoQ, chromium, niacin, riboflavin, polyunsaturated fats, exercise

Pro & antioxidants

therapeutic levels of antioxidants: protect healthy tissue from free radical destruction of chemotherapy & radiation therapy.(i.e. vitamin E, C, beta-carotene, selenium)

certain form and dose of pro-oxidants (i.e. non-heme iron): can accelerate tissue destruction and is sequestered by tumor & pathogens

Anti-proliferative agents

selective toxins for anti-neoplastic activity: i.e. garlic and other minor dietary constituents in plant food

homeostatic mechanism for down regulation of growth: possible role for selenium

anti-angiogenesis factor (hyaluronic acid or other proteins in cartilage, ie. shark cartilage and bovine tracchea)

Influence cell differentiation

retinoids, vitamin D, enzymes

The Protective Action of Vitamins
Against Cancer Include:7

  • preventing the formation of carcinogens
  • increasing detoxification
  • inhibiting transformed cell replication
  • controlling expression of malignancy
  • controlling differentiation processes
  • enhancing cell to cell communication

A Sampling of Cancer Antagonists Found in Varoius Foods (With Active Ingredient in Parentheses)8

inhibitors of covalent DNA binding broccoli & cabbage (phenethyl isothiocyanate) fruits, nuts, berries, seeds, and vegetables (ellagic acid) fruits & vegetables (flavonoids in polyphenolic acid)

inhibitors of tumor promotion orange & yellow fruits & vegetables (retinol) nuts & wheat germ (vitamin E) fruits & vegetables (vitamin C) green, orange, & yellow fruits and vegetables (beta-carotene) garlic & onions (organosulfur compounds, reduce the formation of organosoluble metabolites and increase the formation of water soluble metabolites which are easier to excrete) curry/tumeric (curcumin) chili peppers (capsaicin, a vanillyl alkaloid)

inducing biotransformation cabbage, brussel sprouts, spinach, cauliflower and broccoli (indole-3-carbinol) seafood & garlic (selenium)

reducing the absorption of carcinogens fruits, vegetables, grains & nuts (fiber) fruits & vegetables (riboflavin chlorophyllin)

Nutrients can Reverse Pre-Malignant Lesions

Vitamin C and beta-carotene are effective at reversing cervical dysplasia and oral leukoplakia in humans.9

Vitamin A derivatives (retinoids) reverse bronchial metaplasia in humans.10

Combination of folate and vitamin B-12 reversed bronchial metaplasia in humans.11

Injections of vitamin E, beta-carotene, canthaxanthin (a carotenoid) and algae extract dramatically bolstered levels of tumor necrosis factor alpha and reversed hamster buccal pouch tumors.12

58 adults with familial adenomatous polyps (near 100% progression to cancer if untreated) were entered into a randomized study providing high dose vitamin C with E and high fiber, or placebo plus low fiber diet. The high fiber group experienced a limited degree of polyp regression.13

Nutrients can Inhibit Carcinogenesis

Beta-carotene, vitamin A, C, E reduce the risk of cancer by radiation and chemical carcinogen exposure. Vitamins A, D, and E inhibit the expression of oncogenes.14

Calcium supplements (2000 mg/day) provided a marked suppression of rectal proliferation in experimental but not placebo patients. Calcium seems to markedly inhibit the early stages of colon cancer in genetically vulnerable individuals.15

Taking vitamin supplements was protective against colo-rectal cancer in a large Australian study.16

The former medical director of Sloan Kettering cancer hospital in New York (Robert Good, MD, DSc) has found that many nutrients modulate immune functions and can protect against cancer.17

An extensive book by a former National Cancer Institute oncologist, Dr. Charles Simone, shows the potency of nutrients to prevent cancer.18

Professors at Harvard University have published considerable evidence in the prestigious New England Journal of Medicine showing that 90% of all cancer is environmentally caused and therefore preventable. They cite our 500% higher incidence of breast cancer as being related to diet. They highlight fat, selenium, vitamin A, C, E, and fiber and prime proven nutrition cancer preventers.19

Common Malnutrition in Cancer Patients (and Intervention with Total Parenteral Nutrition, TPN)

A theory has persisted for decades that one could starve the tumor out of the host. Unfortunately, the tumor is quite resistant to starvation. Most studies find more harm to the host than the tumor in either selective or blanket nutrient deficiencies.23 Protein restriction does not affect the composition or growth rate of the tumor, but does restrict host growth rate.24 Folate deprivation allowed the tumor to grow anyway.25 In starved animals, the tumors grew more rapidly than in fed animals, indicating the parasitic tenacity of tumors in the host.26 In animal studies, starving the host led to continued tumor growth and wasting of host tissue.27 Overall, the research shows that starvation provokes host wasting while tumor growth continues unabated.28 Pure malnutrition (cachexia) is responsible for at least 22% and up to 67% of all cancer deaths. While the average “healthy” American is sub-clinically malnourished, the average cancer patient is clinically malnourished. Malnutrition is extremely common in the cancer patient.

Of the 139 lung cancer patients studied, most tested deficient in vitamin C or scorbutic (clinical vitamin C deficiency).29

Another study of cancer patients found that 46% tested scorbutic while 76% were below acceptable levels for serum ascorbate.30

Experts now recommend the value of nutritional supplements, especially in patients who require prolonged TPN support.31

Interleukin-2 therapy induced malnutrition in up to 90% of 20 patients tested. The authors recommend prophylactic nutritional supplements to stem the immune suppression from this iatrogenic malnutrition.32

Recommended Dietary Allowances (RDA) are not designed for cancer patients. Supplements of vitamins, minerals, and other nutrients can benefit the cancer patients.33

Progressive weight loss is common in cancer patients and is a major source of morbidity and mortality.34

Wasting of tissue occurs in hypermetabolic states, most commonly for injury patients and end-stage cancer.35

Chemo and radiation therapy are sufficient stressors in themselves to induce malnutrition.36

Up to 80% of all cancer patients have reduced levels of serum albumin (a leading indicator of protein/calorie malnutrition).37

There is some evidence that tumors are not as flexible in using substrates other than glucose for fuel, hence a low carbohydrate TPN formula may have antineoplastic value.38 A recently published position paper from the American College of Physicians basically stated that TPN had no effect on the outcome of cancer patients.39 Unfortunately, this article selected non-malnourished patients. TPN treats malnutrition, not cancer.40

Weight loss drastically increases the mortality rate for most types of cancer, while also lowering the response to chemotherapy.41

TPN improves tolerance to chemotherapeutic agents and immune responses.42 Of 28 children with advanced malignant disease, 18 received TPN for 28 days with resultant improvements in weight gain, increased serum albumin, and transferrin with major immunological benefits. In comparing cancer patients on TPN versus those trying to nourish themselves by oral intake of food, TPN provided major improvements in calorie, protein, and nutrient intake but did not encourage tumor growth.

27 malnourished cancer patients were provide TPN and had a mortality rate of 11%, while the non-TPN group had a 100% mortality rate.43

Pre-operative TPN in patients undergoing surgery for GI cancer provided general reduction in the incidence of wound infection, pneumonia, major complications, and mortality.44

In one study by Mullen, the patients who were the most malnourished experienced a 33% mortality and 46% morbidity rate, while those least malnourished had a 3% mortality rate with an 8% morbidity rate.

There is evidence that a finely tuned TPN formula can do more than just nourish the patient with broad spectrum nutrient coverage. TPN formulas fortified with arginine have been shown to stimulate the immune system, accelerate wound repair, and promote tumor reduction. Modified diets with low tyrosine (2.4 mg/kg body wt) and low phenylalanine (3.5 mg/kg body wt) were able to elevate natural killer cell activity in 6 of 9 subjects tested.45

In 21 adults on TPN, high amino acid solution (designed for pediatric ICU) with 30% branched chain amino acids was able to provide better nitrogen balance than the conventional 8.5% amino acid TPN formula.46

In 20 adult hospitalized patients on TPN, the mean daily needs (based on urine and serum ascorbate levels) for vitamin C were 975 mg with the range being 350-2250 mg.47

49 patients with small cell bronchogenic carcinoma received chemotherapy with (21 patients) or without (28 patients) TPN. Complete remission was achieved in 85% of the TPN group versus 59% of the non-TPN group.48

In an extensive study of 3,047 cancer patients through the Eastern Cooperative Oncology Group, weight loss was an accurate predictor of poor prognosis.49

Regulate Blood Sugar to Slow Cancer Growth

There is a long-standing well-accepted link between elevated insulin levels and risk of cancer.50

Cancer cells demonstrate a 3 to 5 fold increase in glucose uptake compared to healthy cells.51

Cancer thrives on glucose while also initiating gluconeogenesis and insulin resistance.52 Lipid based parenteral solutions for cancer patients slow cancer growth.

Modest ingestion of glucose (75 gm) caused a measurable decline in cell-mediated immunity in 7 healthy human volunteers. Mechanism of action is probably via elevated insulin, which competes with mitogens for binding sites on lymphocytes.53

In animal studies, progressive increase in sucrose in the diet leads to a dose-dependent decline in antibody production.54

Healthy human volunteers ingested 100 gram portions (average US daily intake) of simple carbohydrates from glucose, fructose, sucrose (white sugar), honey, and orange juice. While simple sugars signficantly impaired the capacity of neutrophils to engulf bacteria, starch ingestion did not have this effect.55

In a study comparing 50 colorectal cancer patients to healthy matched controls, the cancer patients ate considerably more sugar and fat than the healthy people.56

An epidemiological study of 21 countries suggests that high sugar intake is a major risk factor toward breast cancer.57

Animals were fed isocaloric diets of carbohydrates. The group eating more sugar developed significantly more mammary tumors than the starch-fed group.58

Risks of Nutrition Therapy

In an extensive review of the literature, Dr. Adrienne Bendich found the following data on nutrient toxicity59:

  • B-6 can be used at up to 500 mg (250 times RDA) for up to 6 years with safety.
  • Niacin (as nicotinic acid) has been recommended by the National Institute of Health for lowering cholesterol at doses of 3000-6000 mg/day (150-300 times RDA). Time release niacin is more suspect of causing toxicity as liver damage.
  • Vitamin C was tested in eight published studies using double blind placebo controlled design. At 10,000 mg/day for years, vitamin C produced no side effects.
  • High doses of vitamin A (500,000 iu daily) can have acute reversible effects. Teratogenecity is the most likely complication of high dose vitamin A intake.
  • Vitamin E intake at up to 3000 mg/day for prolonged periods has been shown safe.
  • Beta-carotene has been administered for extended periods in humans at doses up to 180 mg (300,000 iu) with no side effects or elevated serum vitamin A levels.

In a separate review of the literature on nutrient toxicity by John Hathcock, PhD, a Food and Drug Administration toxicologist, the following data was reported60:

  • Vitamin A toxicity may start as low as 25,000 iu/day (5 times RDA) in people with impaired liver function via drugs, hepatitis, or protein malnutrition. Otherwise, toxicity for A begins at several hundred thousand iu/day.
  • Beta-carotene given at 180 mg/day (300,000 iu or 60 times RDA) for extended periods produced no toxicity, but mild carotenemia (orange pigmentation of skin).
  • Vitamin E at 300 iu/day (10 times RDA) can trigger nausea, fatigue, and headaches in sensitive individuals. Otherwise, few side effects are seen at up to 3,200 iu/day.
  • B-6 may induce a reversible sensory neuropathy at doses of as low as 300 mg/day in some sensitive individuals. Toxic threshold usually begins at 2000 mg for most individuals.
  • Vitamin C may induce mild and transient gastro-intestinal distress in some sensitive individuals at doses of 1000 mg (16 times RDA). Otherwise, toxicity is very rare at even high doses of vitamin C intake.
  • Zinc supplements at 300 mg (20 times RDA) have been found to impair immune functions and serum lipid profile.
  • Iron intake at 100 mg/day (6 times RDA) will cause iron storage disease in 80% of population. The “window of efficacy” on iron is probably more narrow than with other nutrients.
  • Copper can be toxic, though dose is probably related to the ratio with other trace minerals.
  • Selenium can be toxic at 1-5 mg/kg body weight intake. This would equate to 65 mg/day for the average adult, which is 812 times the RDA of 80 mcg. Some sensitive individuals may develop toxicity at 1000 mcg/day.
  • Manganese can be toxic, though little specific information can be provided for humans.

Adjuvant Nutrition Improves the Effectiveness and/or Reduces the Toxicity from Medical Oncology

Vitamin C enhanced the chemotherapeutic action of levodopa methylester and increased survival time in B16 melanoma-bearing mice.61

Niacin supplementation in animals reduced the cardiotoxicity of the drug without inhibiting the effectiveness of the drug.62

Low serum levels of vitamin A and E were indicative of human cancer patients who responded poorly to chemotherapy.63

50 previously untreated cancer patients randomly received radiation therapy with or without 5 grams/day of vitamin C supplements. After 1 month, 87% of the vitamin C treated group showed a complete response (disappearance of all known disease) compared to 55% of the control.64

Vitamin C and K separately showed anti-tumor activity against human cancer cells in vitro, but became synergistically effective at 2% the regular dosage when used together.65

Vitamin C had no effect on the anti-tumor activity of adriamycin but did prolong the life of the animals treated with adriamycin.66

B-6 deficient mice exhibited enhanced tumor susceptibility and increased tumor size.67

22 patients with precancerous conditions, 19 patients with malignant oral lesions and 13 healthy controls were evaluated with respect to serum selenium levels and response to selenium therapy (300 mcg/day). Using selenium as sole therapy, there was a 38.8% objective response rate in treated patients.68

Human prostatic cancer cells in vitro were markedly inhibited when vitamin E was added to the adriamycin.69

Vitamin E enhanced the growth inhibitory effect of vincristine on mouse melanoma cells.70

Vitamin E therapy (1600 iu/day) begun 5-7 days prior to therapy prevented 69% of adriamycin patients from experiencing baldness.71 Other studies have not always reached the same conclusion but have not followed this protocol. It appears important to begin vitamin E therapy at least 7 days prior to chemotherapy.

Calcium and vitamin D improved the efficacy of thioTEPA and other anti-neoplastic drugs against Hodgkin’s disease and lung cancer.72

Selenium supplements (200 mcg/day) in 23 patients with ovarian cancer or metastatic endometrial cancer showed less host tissue damage than the untreated group.73

A derivative of ascorbic acid (sodium benzylideneascorbate, SBA) was given in daily dose of 200 mg/m2 to 55 patients with inoperable carcinoma. 8 patients achieved a complete response, 21 achieved partial response, 25 remained stable, and 1 showed progression of disease. The activity of this medication was increased with concurrent tamoxifen use.74

While tamoxifen is the commonly used drug to inhibit estrogen-dependent tumor growth, vitamin C has clearly demonstrated the ability to inhibit estrogen-dependent tumor growth in hamsters.75

Vitamin E and selenium helped reduce the lipid peroxidation-induced cardiotoxicity from adriamycin in animal models without inhibiting effectiveness of therapy.76

Potassium bromate can cause nephrotoxicity via renal oxidative DNA damage. In rat model, pre and post treatment with cysteine and glutathione (amino acids) and vitamin C protected against oxidative damage in the kidneys.77

Niacin (vitamin B-3) as nicotinamide is able to dramatically improve the response of hypoxic radioresistant tumors in animal models. Anaerobic tumors do not respond well to radiation therapy, while niacin seems to improve aerobic metabolism to make solid tumors more vulnerable to radiation therapy.78

Vitamin E topically applied (400 mg per lesion, twice daily for 5 days) to oral lesions induced by chemotherapy provided substantial relief in 6 of 9 patients while only 1 of 9 placebo treated patients had any relief from oral mucositis. Vitamin E seemed to best help patients taking cisplatin and 5-fluorouracil. Oral mucositis is often the beginning of anorexia which deteriorates into clinical malnutrition.79

In mouse and guinea pig models, vitamin C prolonged the life of animals treated with adriamycin without affecting the anti-tumor activity of this drug. Vitamin C was able to prevent the adriamycin-induced cardiomyopathy as determined by electron microscopy.80

While tamoxifen is a drug that binds up circulating estrogen, which can incite tumor growth, studies show that wheat fiber does the same thing while also reducing secondary bile acids and bacterial enzymes associated withcolon cancer–without the potential carcinogenic effects of tamoxifen.81

Nutrients have a Profound Impact on the Immune System

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Many nutrients taken orally can provide pharmacological changes in immune function in humans. Protein, arginine, glutamine, omega-6 and omega-3 fats, iron, zinc, vitamins E, C, and A have all been proven to modulate immune functions.82

Vitamin A deficiency causes reduced lymphocyte response to antigens and mitogens, while beta-carotene supplements stimulate immune responses.83

There is extensive literature supporting the importance of vitamin B-6 on the immune system. In one study, B-6 supplements (50 mg/day) provided a measurable improvement in immune functions (T3 and T4 lymphocytes) for 11 healthy well fed older adults.84

Various B vitamins have been linked to the proper functioning of antibody response and cellular immunity.

Folate deficiency decreases mitogenesis.

Deficiency of vitamin C impairs phagocyte functions and cellular immunity.

Vitamin E deficiency decreases antibody response to T-dependent antigens, all of which gets worse with the addition of a selenium deficiency. In test animals, normal vitamin E intake was not adequate to optimize immune functions.85 Modest supplements of vitamin E have been shown to enhance the immune response.

While iron deficiency can blunt immune functions, iron excess can increase the risk for cancer.86

Zinc exerts a major influence on the immune system. Lymphocyte function is seriously depressed and lymphoid tissues undergo general atrophy in zinc-deficient individuals. The lymphocytes in zinc-deficient animals quickly lose their killing abilities (cytotoxicity) and engulfing talents (phagocytosis) for tumor cells and bacteria. Natural killer cell and neutrophil activity is also reduced. All of these compromised immune activities elevate the risk for cancer.

Copper plays a key role in the production of superoxide dismutase and cytochrome systems in the mitochondria. Hence, a deficiency of copper is manifested in a depressed immune system, specifically reduced microbicidal activity of granulocytes.

Selenium works in conjunction with vitamin E to shield host cells from lipid peroxidation. Humoral immune response is depressed in selenium deficient animals. Selenium and vitamin E deficiencies lead to increased incidence of enteric lesions. Lymphocyte proliferation is reduced in selenium deficiency. The theory is that selenium and vitamin E help to provide the host immune cells with some type of “bullet proof plating” against the toxins used on foreign cells. Hence, one immune body can live on to destroy many invaders if enough vitamin E and selenium allow for these critical chemical shields.

In magnesium deficiency, all immunoglobulins (except IgE) are reduced, along with the number of antibody forming cells. Magnesium is crucial for lymphocyte growth (involvement in protein metabolism) and transformation in response to mitogens. Prolonged magnesium deficiency in animals leads to the development of lymphomas and leukemia.

Iodine plays an important role in the microbicidal activity of polymorphonuclear leukocytes. Activated neutrophils may use the conversion of iodide to iodine to generate free radicals for killing foreign invaders.

Boron is an interesting trace mineral, since it is now recognized for its role in preventing osteoporosis, yet is still not considered an essential mineral. Boron deficiency in chicks creates immune abnormalities like arthritis.

Toxic trace minerals, like cadmium, arsenic and lead all blunt the immune system.

The quality and quantity of fat in the diet plays a major role in dictating the health of the immune system. A deficiency of the essential fatty acid (linoleic acid) will lead to atrophy of lymphoid tissue and a depressed antibody response. And yet excess intake of polyunsaturated fatty acids will also diminish T-cell immune responsiveness. Since fat directly affects prostaglandin pathways, and prostaglandins (depending on the pathway) can either depress or enhance immune function, fat intake is crucial in encouraging a healthy immune system. Oxidized cholesterol is highly immuno-suppressive. Cholesterol is less likely to oxidize while in the presence of anti-oxidants, like vitamin E, C, and beta-carotene.

Basically, nutrition plays a key role in the effectiveness of the immune system. Primary assessment techniques to find the relative nutrient status of the immune system include:

  • Clinical: dietary intake, physical examination
  • Anthropometric: skin fold thickness, percent body fat
  • Hematologic: hemoglobin and ferritin levels
  • Biochemical: serum albumin, serum transferrin, creatinine/height index, zinc status
  • Immunologic: lymphocyte count, terminal transferase activity, T-cells
  • Miscellaneous: hand grip strength, dark adaptation, taste acuity

A main goal of this nutrition program is to optimize the functioning of the immune system via foods and nutritional supplementation (pills, powder, or TPN). A healthy immune system is better able to join in the battle to rid the body of tumor cells.

Therapeutic Supplements may help Cance Patients

Vitamin E.

Was used (via injections) to reverse oral tumor progress in animals with induced tumors.89

Prevents and may even reverse tumor growth in animals with chemically induced tumors.90

Was able to prevent expected tumors in lab animals exposed to DMBA.91

Increased the effectiveness and specific toxicity of chemotherapy agents on tumors in culture.92

Relieves most cystic breast disease, which indicates that E can treat pre-cancerous conditions.93

May be anti-neoplastic by virtue of its ability to protect the prostaglandin prostacyclin.94

Protects against damage from radiation therapy.95

In combination with selenium was able to prevent expected tumors in animals after DMBA injections.

Significantly elevated the microsomal hydroperoxidase activity.96

And selenium provided partial protection against cardiotoxicity in adriamycin use on rabbits. Best protection was aforded by high dose vitamin E.97

Deficiency accentuated the cardiotoxicity of adriamycin in rats.98

Increased (in vitro) the therapeutic benefits of chemotherapy agents on human prostate cancer cells.99

Directly stunted the growth of mouse melanoma cells in vitro.100

Topical application of DMSO and vitamin E produced a 68% decrease in skin necrosis on mice given adriamycin.101

Mice with oral cancer were supplemented with injections of vitamin E, beta-carotene, canthaxanthin, and algae extract. Major improvements in tumor necrosis factor were measured in the supplemented mice, who also experienced varying levels of tumor regression.102

Reduced the cardiotoxic effects of daunomycin (similar to adriamycin) in test animals.103

And vitamin K3 (menadione) enhanced the anti-metabolic activity of the chemotherapy agents 5FU and leucovorin in vitro.104

Sensitized tumor cells, but not healthy cells, to radiation therapy for enhanced effectiveness.105

Use in radiation therapy reduces toxic side effects.106

Patients with peripheral neuropathy (common as a side effect for certain chemo agents) were found to be clinically low in vitamin E in the region of nerve damage.107 Nerve numbness in cancer patients may be due to the elevated need for vitamin E during chemotherapy.

Elevates lymphocyte proliferation in animals.108

Vitamin E, A, and prenylamine blunted the cardiotoxic effects of adriamycin in rabbits.109

Provided measurable protection against the cardiotoxicity of adriamycin in rabbits.110

Using 1600 iu/day of vitamin E, hair loss in cancer patients was reduced from the typical 90% to 30% in the treated group.111

Toxicity. Human studies show no side effects from vitamin E at levels up to 3200 mg/day (3200 iu/day).112

Vitamin K

The primary function of K is as a coagulating factor in the prothrombin cascade in the blood. A normal diet combined with bacterial fermentation in the distal small bowel appears to provide “adequate” levels of K to prevent hemorrhage.113

Normal daily intake is difficult to estimate since an undetermined amount of K is produced through bacterial fermentation. However, the National Academy of Sciences estimates that the average American diet contains 300-500 mcg/day. 114

Vitamin K exists in 3 distinct chemical analog forms with the following differences

K-1 (phylloquine or phytonadione, relatively non-toxic, preferred form for non-pharmacological purposes)

K-2 (menaquinone, produced by bacterial fermentation in the gut, does not inhibit DNA synthesis in malignant cells)

K-3 (menadione, synthetic derivation, accumulates in the liver, can be toxic, is most effective as an anti-neoplastic agent).

Additionally, over the past thirty years, evidence has been gathering that K has anti-neoplastic properties. 115

Common deficiencies.

K deficiency is common in patients with general malnutrition, intestinal malabsorption, or treatment with anti-biotics.116

A profound deficiency of vitamin K was found in 34 cancer patients on anti-microbial therapy.117

Therapeutic doses of vitamin E elevate the need for vitamin K.118

Therapeutic levels required to reverse hemorrhagic clinical vitamin K deficiency range from 20-50 mg/day of K.

Use in cancer treatment.

When vitamin K (as Synkavite, menadione, K-3) was given to human cancer patients IV at a 50-100 mg dosage prior to radiation therapy, 5 year survival increased from 20% of the patients without K to 39% of the matched group given radiation plus vitamin K. 119


Vitamin K-1 (not K-3) supplements will reduce the effectiveness of anti-coagulants at lengthening prothrombin clotting time. Vitamin K-1 (phytonadione) at 1 mg/day does not present any hazard to patients receiving anti-coagulant therapy.120 According to Dr. Chlebowski, vitamin K enhances the anti-metastatic effects of anti-coagulants.

Vitamin C.

In animals with implanted Ehrlich carcinoma and L1210 leukemia, injections of vitamin B-12 (hydroxocobalamin) and vitamin C (dehydroascorbic acid) provided dramatic improvements in survival of the animals. By day 19, all 20 of the control animals were dead, while 50% of the treated mice survived 60 days or more. This nutrient combination has a precedence for limiting tumor growth without affecting the host.121

Potentiates the value while reducing the toxicity of chemotherapy in animal studies.122

Potentiates the value of radiation therapy.123

Using chemotherapy in conjunction with nutritional therapy, supplemental levels of vitamins A (Aquasol A 400,000 iu/day), C (8 gm/day), and E (3200 iu/day) were provided to 20 cancer patients over the course of 12 months with 7 (35%) experiencing complete remission, 8 (40%) partial remission, and 5 (25%) failed. Only one patient experienced any symptoms attributed to the mega-vitamin therapy.124

Mice with induced liver cancer were then pre-treated with vitamins C and K3 (menadione) before using various chemotherapy drugs. The nutrients provided considerable protection while enhancing the effectiveness of the treatment.125 Postulated mechanisms include the attack on catalase-deficient cancer cells by the combination of vitamin C and K3.

Vitamin C, thiamin, and cysteine provided nearly complete protection against free radical acetylaldehyde destruction in animals.126

Vitamin C (10 gram/day) provided life extension and improvement of quality of life in 100 terminal cancer patients.127 Other studies have not had such promising results. Possible explanations for the discrepancy may be that the other studies used patients who had been heavily pre-treated with chemo and radiation therapy and considered unresponsive and terminal.

Vitamin C and E provide measurable protection against the carcinogen PCB in various animals.128

2-3 grams daily of ascorbate provided stimulation of lymphocyte transformation to certain mitogens.129

After 9-12 months on 3 grams daily of vitamin C supplements, rectal polyps were reduced in the treated group by 74% compared to the untreated group reduction of 31%.130

Ascorbic acid supplements in cancer patients provided improvements in minor symptoms, pain control, and quality of life.131

Vitamin C supplements provided protection against the cytotoxic effects of methotrexate in mice.132

Toxicity. Most patients can tolerate 10-20 grams orally. Other patients will experience mild intestinal distress at these levels. Up to 100 grams has been used in TPN formulas.


Quercetin increased the cell kill rate in cancer cells (in vitro) exposed to hyperthermia (heat therapy) with no effect on normal healthy cells.133

Quercetin inhibited cancer in animals exposed to two carcinogens.134

Quercetin caused inhibition of growth (in vivo) in two squamous cell carcinoma lines.135

Several bioflavonoids (including quercetin) were able to inhibit DNA binding from benzopyrenes. 136

Vitamin A

Of 102 people who had bladder cancer, the incidence of recurring tumors was 1.8 times higher in those who consumed the lower amounts of vitamin A.137

Nine male patients with metastatic unresectable squamous cell carcinoma of the lung were treated with vitamin A palmitate or 13 cis-retinoic acid (analog of vitamin A) without other medical intervention. 60 weeks later, immune function had improved and progress against the tumor had been made.138

Vitamin A in combination with BCG suppressed tumor growth in the lung tumors of animals. Vitamin A alone did not affect tumor growth, but only in conjunction with BCG.139

Vitamin A prevented impaired wound healing in post-operative and irradiated rats. Vitamin A provided continuous high level of immune competence throughout the normal immunosuppressive phase.140

Vitamin A supplements provided complete or partial remission in patients with benign breast disease.141

Toxicity. 300,000 iu/day of retinol palmitate (preformed vitamin A) administered to 138 lung cancer patients for at least 12 months produced occasional dry skin, but no significant side effects.142 Toxicity may begin at levels of 500,000 iu/day (100 times the RDA) long term intake for adults, and proportionately less in children.143 Toxicity usually involves consumption of 200,000 iu/day for many days, though individuals with compromised immune function may develop toxicity at 25,000 iu.144 Toxicity of A can be reduced by higher intake of vitamin E to mitigate lipid peroxide effects.

Beta carotene

2500 iu of beta-carotene = 250 retinol equivalents =1.5 mg. Beta-carotene has been shown to protect phagocytic cells from auto-oxidative damage, enhance T and B lymphocyte proliferation, enhance macrophages, interleukin production, and natural killer cell tumoricidal abilities.145

Beta-carotene probably has effectiveness against cancer as a chain-breaking anti-oxidant.146

Vitamin A intake protected workers who were smokers and/or exposed to toxic chemicals against lung cancer. Beta-carotene provided a more protective edge than animal sources of vitamin A.147

Using combined supplements of beta-carotene and canthaxanthin, Italian researchers found that cancer patients who had undergone surgery with radiation therapy had a much higher than anticipated survival rate and level of health.

A review of the literature on vitamin A and beta-carotene shows that beta-carotene has anti-oxidant and immune stimulating properties that are not found in vitamin A. Perhaps these are two distinct nutrients.148

Beta-carotene has been shown to protect animals against ultra-violet induced skin tumors and carcinogen treatment by preventing malignant transformation and nuclear damage.149

Beta-carotene and algae extracts injected into DMBA-provoked tumors in hamsters caused regression of the tumors.150

Toxicity. Toxicity of beta-carotene has never been found, since it is not mutagenic, carcinogenic, embryotoxic, or teratogenic and does not cause hypervitaminosis A.151

15 mg daily of oral supplements of beta-carotene (25,000 iu.) provided a 10 fold increase in serum beta-carotene without any skin discoloration.152

People have consumed 300,000 iu (180 mg) of beta-carotene daily for 15 years with no adverse side effects. In the few beta-carotene reactions, it is always with excess consumption of food components (like carrot juice), which makes other food components and not the beta-carotene suspect in these mild toxicity reactions. Pure beta-carotene supplements have never produced toxicity in any human studies.

B-6 (pyridoxine)

While earlier findings indicated that a B-6 deficiency would slow down tumor growth153 and increase survival in animals with cancer154, more recent findings indicate the opposite. Animals fortified with B-6 and then injected with melanoma cells showed a greater resistance to this deadly form of cancer.155

B-6 inhibited melanoma cells in vivo.156

Vitamin B-6 displays important immune modulating activity of the immune system.157

Vitamin B-6 at 25 mg/day for 33 bladder cancer patients provided marked improvement in cancer recurrence over the control group.158

Vitamin B-6 kills hepatoma cells (in vitro).159

Administered as an ointment on a human melanoma patient four times daily for a two week period resulted in disappearance of the cutaneous papules.160

High dose supplements (300 mg/day) provided considerable relief from the toxicity of radiation therapy.161

Pyridoxine deficiency produces increased tumor resistance.162

Newly diagnosed children with leukemia have suboptimal overall nutrition as well as suboptimal vitamin B-6 status.163

B-6 inhibits the growth of human malignant melanoma cell line.164

B-6 significantly inhibited melanoma cells lines (in vitro) and may be an effective anti-neoplastic agent.165

B-6 (300 mg/day) administered throughout the 8 week radiation therapy course for human endometrial cancer patients improved survival by 15% at 5 years.166

Toxicity. Less than 500 mg/day in humans appears to be safe.167 300 mg/day provide maximal protection against radiation therapy.



High dose supplementation (equivalent to 54 mg/day in humans) resulted in 83-90% reduction in the rate of tumor growth in mice.168

In mice fed either a high or low PUFA fat diet, selenium provoked a drop in tumor incidence in both groups. Selenium apparently exerts a cancer-protective role beyond its antioxidant function in lipid metabolism.169

Enhanced drug detoxification pathways (conjugative, not by P450) in animals.170

Reduces the toxicity of paraquat (an herbicide).171

In animal studies could (a) inhibit both the initiation and promotion phases of cancer, (b) continuous intake of selenium was necessary to achieve maximum protection, (c) inhibit the re-appearance of tumors after surgery.172

Provided fewer DNA strand breaks and greater repair of broken DNA than unsupplemented or less supplemented hamsters.173

Administration of sodium selenite (equivalent to 120 mg for an adult) inhibited the growth of leukemia cells and increased the longevity of test mice.174

Mega-doses effectively limited tumor growth in mice with Ehrlich ascites tumors. Although high dose selenium supplementation did not affect the growth of healthy normal animals, it did have a definite retarding effect on rapidly dividing cells.175 Selenium may be an important anti-proliferative factor to squelch rapidly dividing tumor cells.

Provided considerable protection against the toxic effects of cis-platinum, allowing the lethal dose to kill half the animals (LD50) to increase from 9.3 to 17.5 mg/kg, thus allowing higher and more effective doses of chemotherapeutic agents.176

In mice provided measurable improvements in natural killer cytotoxicity in spleen cells (70% improvement over unsupplemented mice), specific T-lymphocyte cytotoxicity, and other immune parameters that could be therapeutic against cancer.177

Toxicity. The National Academy of Sciences indicates that long-term daily intake of 5000 micrograms of selenium may result in fingernail changes and hair loss. Extrapolated from animal studies, 7 mg (7000 mcg) in humans may halt tumor progression. Selenite is more toxic than selenium bound to amino acids (i.e. selenomethionine). Ingestion of 1-5 mg/kg body weight of selenite will likely produce toxic side effects (65,000 mcg in the 65 kg adult).


EPA (eicosapentaenoic acid).

A diet high in menhaden oil (20% of kcal) promoted major increases in cytochrome P450 in test animals.178

For one week pre-operative and 4 weeks after tumor implantation, varying levels of EPA and DHA from fish oil induced significant reduction in the weight and volume of the implanted mammary tumors in test animals.179

EPA slowed tumor growth in mice with inoculated human colon cancer.180

EPA slowed tumor growth and prolonged survival in mice with transplanted human metastatic breast cancer.181

EPA in conjunction with anti-human milk fat globule monoclonal antibodies offered the greatest reduction in tumor size (36% below corn oil or lard diets) in mice innoculated with human breast tumors.182

EPA diet significantly lowered the level of estradiol (a putative breast tumor marker) in 25 women at risk for breast cancer.183

EPA has protective effects against the development and/or progression of various animal tumor models studied.184

EPA produced a significant decrease in the development of both the size and number of preneoplastic lesions in animals in induced tumors.185

EPA reduced the size and number of tumors while increasing the tumor latent period in rats fed various types of fat in the diet, then exposed to carcinogens.186

EPA-fed rats had significant reduction in the growth of induced tumors.187

EPA-fed mice had significant slowing of tumor growth.188

EPA slowed tumor growth in transplanted mammary tumors in rats.189

EPA inhibited the development of tumors in athymic mice inoculated with human breast cancer. EPA also had a synergistic effect with Iodine 131 labeled monoclonal antibodies in reducing tumorogenesis.190

EPA rich diet significantly depressed growth rate of human breast tumors transplanted into animals. Tumors in EPA-fed animals are more responsive to chemotherapy agents (mitomycin C, doxorubicin).191

EPA reduced tumor growth in transplanted human colon cancer into mice.192

EPA-fed animals had fewer and smaller lesions after induced cancer.193

EPA slowed tumor growth in animals even when administered several months after tumor induction.194

EPA reduced the weight and volume of tumors in transplanted human prostatic cancer to animals.195

EPA retarded the development of human prostatic cancer that was inoculated in animals.196

EPA reduced both the frequency and rate of metastasis of transplanted tumors in animals.197

EPA improves the response of tumor cells to hyperthermia and chemotherapeutic agents by altering the properties of the tumor cell membrane.198

EPA increases the adriamycin kill rate on cultured human leukemia cells.199

EPA substantially reduced the invasiveness of cultured human tumor cells (both malignant murine melanoma and fibrosarcoma).200

EPA and GLA separately were able to selectively kill cultured human tumor cells.201

EPA and GLA enhanced the tumoricidal effects of anticancer agents in vitro.202

EPA and GLA were selectively toxic to human breast, lung, and prostate cancer cells in vitro. The fatty acids also enhanced the cytotoxic activity of cytotoxic drugs on tumor cells.203

EPA and GLA suppressed the growth of cultured human larynx cancer cells.204

DHA (accompanying fatty acid with EPA in fish oil) was able to partially reverse adriamycin-resistant small cell lung carcinoma cells in vitro.205

EPA modulates estrogen metabolism for reduced risk in breast cancer.206

EPA rich diet can slow tumor growth through modulation of both tumor protein synthesis and breakdown.207

EPA may have a beneficial role as adjunctive anti-neoplastic therapy in breast cancer.208

EPA provided higher survival (7 of 11 versus 2 of 11 in control group) of guinea pigs injected with endotoxin209.

EPA provided higher survival (87% versus 63% in control group) for guinea pigs injected with endotoxin.210

EPA provided higher survival (83% versus 50% in control group) for guinea pigs injected with endotoxin.211

How Does the EPA Slow Tumor Growth?
Proposed Mechanisms

Altering membrane fluidity in healthy and/or tumor cells to change the basic cellular metabolism.

By altering membrane fluidity, can change the response of tumor cells to growth factors, hormones, antibodies.

Alters prostaglandin output, with more anti-inflammatory and anti-aggregatory eicosanoids.

Perhaps by prostaglandin metabolism, reduces the “stickiness” (aggregation) of cancer cells, to retard their metastatic abilities. Amount of EPA necessary for the average adult to have measurable reduction in cell aggregation (stickiness): 2-4 gm/day. Gorlin, R., Archives of Internal Medicine, vol.148, p.2043, Sept.1988

Stimulates the immume system.

Alters bile acid metabolism (may be important in colon cancer).

May be directly toxic to tumor cells, which have altered capacity to use any type of fats. Without proper use of fat soluble antioxidants, tumor cells may find the highly unsaturated fatty acids of EPA to be like an internal “hand grenade”.

Attenuates shock from lactic acidosis in endotoxin-exposed animals. May buffer the impact of cytotoxic drugs on human cancer patients.

Alters hormonal balance for estrogen and testosterone dependent tumors.

Counterindications for the use of EPA

Can induce vitamin E deficiency, unless supplements of E are added. Suggested dosage: 400 iu vitamin E per every 2500 mg EPA.

Reduces platelet aggregation and slows normal blood clotting. High dose counterindicated for patients anticipating surgery.

Yetiv, JZ, Journal of the American Medical Association, vol.260, p.665, Aug.5, 1988

Toxicity A one gram capsule of fish oil usually provides 240-600 mg of EPA. Intake of 6000 mg of EPA may inhibit blood clotting, hence may be counterindicated in patients due for surgery. A minimum of 1000 mg daily of EPA must be consumed to expect any beneficial effects. EPA to GLA in a ratio of 5:1 may encourage the production of prostaglandin PGE-1 for immune stimulating effects.

GLA (gamma linolenic acid)

Combined intake with vitamin C was able to double the mean survival time for patients with primary hepatic carcinoma.212

Provided subjective and objective improvements in 21 patients with untreatable malignancies.213

GLA plus iron supplements dramatically increased the tumor cell kill rate with in vitro studies on human cancers, opening the possibility to a relatively safe and selectively toxic cancer regimen.214

Varying combinations of GLA and EPA were able to provide a high cancer cell kill rate in vitro.215

Toxicity. A one gram capsule of evening primrose oil provides about 200 mg of GLA. Intake of 600 to 3000 mg of GLA may bring about favorable results in the cancer patient.



Animals fed arginine rich diets (5%) had considerably fewer and more benign tumors when later treated with the carcinogen DMBA.216

Arginine added to drinking water in animals was able to inhibit subcutaneous tumor growth.217

Arginine added to diet of mice (5% of wt.) produced fewer tumors, slower growing tumors, and twice the mean survival time as compared to untreated mice.218

Via animal studies, researchers have speculated on two primary functions of arginine in the body: essential for the synthesis of reparative collagen in wound recovery, decreases some of the negative aspects of metabolic responses to injury.219

Arginine supplements in animals stimulated thymus activity which resulted in reduced tumor growth.220 Arginine also dramatically improves wound healing.

Arginine stimulates lymphocyte immune response in 21 healthy human volunteers.221

Arginine supplements in tumor-bearing mice provided enhanced T-cell function, increased response to autologous tumors, retarded tumor growth, and prolonged median survival time.222

In mice with neuroblastomas, arginine supplements provided significant tumor retardation in the immunogenic group.223 Arginine’s tumoricidal abilities go beyond its protein sparing abilities or immune stimulation.

Arginine supplements in mice provided significant enhancement of cytotoxic T-lymphocytes, natural killer cell activity, interleukin-2 receptors and general immune improvements.224

Toxicity. At therapeutic levels (above 5 grams/day) may activate growth of certain viruses.

n Branched chain amino acids (leucine, isoleucine, valine)

Accelerates protein synthesis and elevates albumin synthesis from 8.5% to 19.7% when used in TPN formula in 10 malnourished cancer patients.225

Cysteine (N-acetylcysteine)

Cysteine enters into various detoxification systems in the body. Can be converted to glutathione, which may become GSH, a potent broad spectrum anti-oxidant enzyme system. May reduce the toxicity of chemotherapeutic agents. N-acetylcysteine neutralizes a toxic by-product (acrolein) of cyclophosphamide therapy, hence preventing harm while allowing the effectiveness.226

N-acetylcysteine may neutralize the effectiveness of adriamycin while preventing the cardiotoxicity effects.227

N-acetylcysteine reduced the cardiotoxicity of doxorubicin in dogs.228

N-acetylcysteine blocked the cardiotoxicity of doxorubicin but did not affect the uptake or metabolism of the drug in the heart or liver.229

Acetylcysteine prevented the hemorrhagic cystitis that usually appears from ifosfamide administration.230

Topical application of N-acetylcysteine ointment may reduce toxic side effects (skin reactions, hair loss, damage to mucus membranes of the eyes) from radiation therapy.231

Cysteine supplements promoted glutathione synthesis, which resulted in protection from the toxic effects of acetaminophen in mice.232

Toxicity. Although safe in dosages up to 10 grams/day, the nauseating taste and smell can cause vomiting. Normal dosage is 2-3 grams every 6 hours.


Methionine supplements reduced the uptake of mercury in test animals.233 This may help reduce the amount of toxins (chemotherapy) stored in healthy tissue.


Green tea.

Tea catechins (tannins) are potent inhibitors of platelet aggregation in rabbit platelets.234

Green tea is a more potent scavenger of free radicals than vitamin C or E.235

Green tea contains potent anti-carcinogenic agents.236

Green tea was able to inhibit tumor initiation and promotion in animals.237

Maitake mushroom

Oral administration of maitake mushroom extract (Grifola frondosa) completely inhibited tumor growth in animals.238

Intraperitoneal injections of Maitake in tumor-induced animals showed an increase in cytostatic activity toward syngeneic tumor cells.239

Maitake supplements potentiated host-mediated antitumor activity in mice.240

Intraperitoneal injections of Maitake extract into tumor-induced animals showed marked inhibitory activity on the growth of solid form sarcoma.241

n Plant phytosterols

Phytosterols in plants reduce the risk for colon cancer through a variety of factors.242

Plant carotenoids

A plant dormancy hormone and vitamin A analog (abscisic acid) showed profound anti-tumor activity in rats.243

Cartilage anti-angiogenesis factor

Inhibits tumor growth by preventing the tumor from developing an expanded circulatory network.244

Angiogenesis may be a key marker of tumor progression in 30 patients with malignancies and 19 without.245

There is an induction of angiogenesis during the transition from hyperplasia to neoplasia.246

A cartilage extract (Catrix) was able to markedly inhibit human tumor cell line growth from 22 different patients with malignancies.247

Extract of shark cartilage inhibited tumor growth in vivo.248

Infusion of cartilage extract markedly reduced tumor growth in animals.249

An isolated fraction of cartilage inhibited tumor neovascularization.250

Inhibition of vascularization via a factor in cartilage slows tumor growth.251

Cartilage extract inhibits neo-vascularization (growth of new blood vessels).252

Catrix (preparation of bovine tracheal cartilage rings) was able to provide improvement in 90% of patients and complete remission in 61% of 31 cancer patients given first injections and then oral supplements (eight 375 mg caps every 8 hrs). There was no evidence of toxicity.253

An extract of shark cartilage was used to prevent tumor growth in implanted cornea tumors in rabbits.254 It could be that the extremely low incidence of tumors in sharks is due to the high presence of this cartilage anti-angiogenesis factor.

Calf scapular cartilage inhibited and reversed tumor growth for implanted tumors in rabbits and mice. No toxic effects were observed.255

Toxicity. No toxicity observed.


May protect against enteritis resultant from radiation therapy.256


Highest sources are mother’s milk, human bone marrow, and shark oil. Shown to enhance the regression of uterine cancer when administered prior to radiation therapy.257

Use of alkylglycerols prior to, during, and after radiation therapy reduced injuries by as much as two thirds.258

Coenzyme Q.

Reduces adverse side effects of chemotherapy with adriamycin, including cardiac output, anginal symptoms, and EKG abnormalities. Hair loss was also reduced.259


Neither an essential nor toxic mineral, cesium therapy is able to slightly alter the pH of the cancer cells to make them more vulnerable to immune attack.260

Maharishi-4 (an herbal preparation, ayurvedic food supplement)

Mice who were treated with M-4, then exposed to DMBA had reduced incidence and multiplicity of tumors. Those M-4 treated mice who did get cancer showed tumor regression in 60% of cases within 4 weeks.261

Nucleic acids (RNA/DNA)

In protein depletion, RNA supplements may be mandatory in order to return immune functions to normal.262


Fatty acids: serum fatty acid profile (both volumetric and germane ratios) are accurate indicators of metastatic progress.263 This test provides guidance for adjusting dietary fat intake, test available from Center for Human Functioning (316-682-3100) or Metametrix (800-221-4640).

Allergies: An overloaded immune system is compromised in its ability to destroy tumor cells. The debate continues on which is the best allergy test. ELISA/ACT measures immune delayed type hypersensitivity (Serammune 800-553-5472); Elisa measures IgE and IgG levels (Immuno Labs 800-231-9197).

Immune capability. Natural Killer cells are generally recognized as the most predictive aspect of the tumor killing capacity of the human immune system. Send blood sample to ImmunoSciences Lab (800-950-4686)

General diagnostics. Various tests at International Diagnostics (800-622-2343) or Metametrix

Vitamins (functional assay of enzymatic activity): by Metametrix (800-221-4640), or Pantox (619-272-3885), or Doctor’s Data (800-323-2784)

C-strip: litmus paper dipped in fresh urine to indicate ascorbic acid content of blood (at or near saturation level) from Seraphim (800-525-7372)

Minerals: Provocative assay via chelating agent inducing urinary excretion. Volumetric and germane ratio recorded from Doctor’s Data (800-323-2784)

Venous pH: Mild variations from normal indicate need for balancing using acid or alkaline diet.

Percent body fat by Futrex (800-545-1950) indicates serious long term lean tissue wasting or obesity that may accelerate tumor growth

Indirect calorimetry (INDC): Measures oxygen consumed and carbon dioxide exhaled to determine exact metabolic needs for calories. Essential test in cachectic TPN patients. Also called Metabolic Cart

Skin patch anergy test: indicates overall responsiveness of immune system

Oxidative stress: breath pentane as measured on gas chromatograph helps guide the balance between pro-oxidants (chemo & radiation) and anti-oxidants (nutrients)

Questionnaire: Quality of life indicators which help to track overall response from therapy.

Computer diet analysis: Helps educate patient on errant dietary habits by comparing patient’s dietary intake with accepted standards of nutrient intake.

Digestion: Heidelberg capsule which is swallowed, then transmits the pH of the stomach and intestines to a nearby receiver (Heidelberg 404-449-4888)

Digestion, absorption, intestinal parasites: Send stool sample to appropriate labs.

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