Nutrition & Cancer
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



Technical


ADJUVANT NUTRITION IN CANCER TREATMENT, by Patrick Quillin,
PhD,RD

VITAMINS AND CANCER by Frank Meyskens, MD

VITAMINS AND MINERALS IN THE PREVENTION AND TREATMENT OF CANCER by Maryce
Jacobs, PhD

MODULATION AND MEDIATION OF CANCER BY VITAMINS, by Frank Meyskens, MD

ESSENTIAL NUTRIENTS IN CARCINOGENESIS, by Lionel Poirier



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



Bioenergetics



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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Petrie, HT, Selenium and the immune response: Enhancement of murine cytotoxic
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July 1990



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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


VITAMINS

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



Counterindications.



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.



Bioflavonoids



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.



MINERALS



Selenium.



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).



FATTY ACIDS



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.



AMINO ACIDS



Arginine.



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.



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



OTHER NUTRIENT FACTORS



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.



Glutamine.



May protect against enteritis resultant from radiation therapy.256



Alkylglycerols
.



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



Cesium.



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



ASSESSMENT



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.


Avatar Written by Patrick Quillin PhD RD

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