Dana Myatt, N.M.D. and Mark Ziemann, R.N.

Overview

Some types of cancer are consistently responsive to conventional medical treatment, especially those amenable to surgical intervention when diagnosed early. Cytotoxic therapy is helpful in selected instances. For most cancers, especially those advanced beyond Stage I or II, conventional treatments that evoke durable remissions are elusive and inconsistent. In many instances, cytotoxic and radiation therapies end a patient’s life sooner than the natural course of the disease would be expected to.

Alternative cancer therapies, while typically gentler and less inherently dangerous, have also proven inconsistent for evoking durable remissions. However, instances can be found where durable remissions and event apparent cure have been obtained by unconventional and alternative treatments used as stand-alone therapy. When used in conjunction with conventional treatments, alternative therapies can sometimes potentiate the positive effects of conventional therapy, mitigate the negative effects, or both.

The questions we will examine in this presentation include:

I.) Which alternative treatments are most effective as the sole treatment for malignancy and when should they be used?

II.) Which alternative treatments are most effective as adjuncts to conventional therapy?

III.) Which alternative treatments may be contraindicated for adjunct cancer therapy?

A careful review of the medical literature reveals that there are in fact specific modes of action to explain when and why alternative treatments are effective and when such treatments fail.

Cancer Cell Characteristics: Understanding the Enemy

Developing a cohesive and effective treatment strategy requires an understanding of the behavior and biology of cancer cells. Although various cancer types display unique behaviors, there are a number of characteristics common to all solid tissue malignancies:

1. Altered interactions with neighboring cells. Unlike normal cells whose division stops when neighboring cells are encountered, cancer cells continue to multiply with uncontrolled growth. This trait is known as lack of contact inhibition.

Normal cells require a solid substrate (basement membrane) upon which to grow. This is known as anchorage-dependent growth. Cancer cells are anchorage-independent, growing in circumstances where they are deprived of substrate.

2. Altered cellular metabolism. Cancer cells demonstrate a greatly increased rate of glucose transport. Anaerobic glycolysis is the predominant energy pathway of cancer cells, even in the presence of adequate oxygen. This may partly explain the large amount of metabolic acids produced by cancer cells.

Tumor cells have reduced growth requirements and will proliferate in culture media (less than 1% serum) that halt cell growth and division of normal cells.

3. Vascularization. Tumor cells secrete angiogenic growth factors which cause non-neoplastic blood vessels to grow from surrounding normal tissue. Research indicates that associated fibrin deposits many be necessary for angiogenesis. (1,2)

4. Invasion and metastasis. Multiple characteristics allow for local invasion and distant metastasis.

Cancer cells often secrete enzymes including collagenase, heparinase and stromolysin which are capable of degrading basement membrane and allowing invasion of tumor into adjacent tissues and general circulation.

Inflammation is caused by cellular substances, high acid cellular waste, and tumor pressure on adjacent normal tissue which produces histamine, leukotrienes and prostaglandins of the 2 series, increasing capillary permeability.

Anchorage independence (discussed above) allows cancer cells to travel through the blood stream without substrate. Normal cells do not have this ability. Once a clump of cancerous sells has made its way into general circulation, aggregates of platelets and/or fibrin encasement may serve as protection from the immune system.

Cancer cells have affinity for metastasis to certain and predictable locations not related to obvious blood flow patterns. Unidentified tissue chemotactic factors or lectin binding sites may account for this attraction. (3)

5. Escape from immune surveillance. Carcinogenic burden may simply overwhelm available immune surveillance, especially in the immunocompromised host.

Many cancer patients have apparently intact immune systems, however, and it is felt that cancer cells may secrete substances which circumvent the host’s immune response. Such immune-eluding substances include prostaglandins and other inflammatory substances. Fibrin and platelet aggregation may also serve to assist in protection from host immune response.

Tumor cells also appear to escape host immunity by down-regulation of Human Leukocytic Antigen (HLA) expression. HLA assists lymphocyte recognition of target cells.

Causes of Cancer

Understanding the causes of a particular cancer gives valuable clues to vulnerabilities and points of attack. Immune system dysfunction has long been considered a primary cause and point of treatment in alternative cancer treatment. However, there is significant evidence to suggest that immune dysfunction is only one of a number of causative factors and certainly NOT the most important one.

It appears that very few cancers have a single cause or “initiator.” Instead, most cancers may begin as a series of combination of events that lead to mutation. Tumor initiation begins when DNA in a cell or population of cells is damaged by exposure to exogenous or endogenous carcinogens. This alone is not sufficient to give rise to cancer. Damage at this point can be repaired. If DNA damage is not repaired or damaged cells eliminated, and if the microenvironment of the damaged calls are suitable to contribute to cell growth, then the process continues to the “promotion” phase. (48,49,50,51,52)

Known initiators of cancer include:

1. Genetic factors. A number of genetic factors may play a role in susceptibility to cancer, although study of this aspect of malignancy is a newly emerging field. (47) Such genetic factors include APC/MCC (45,46), RAS, DCC, p53 mutations and/or allelic losses, hyperexpression of c-MYC and RB genes. (10)

Mutation of the p53 tumor suppressor gene is the most frequently observed genetic lesion in human cancer; more than 50% of all human tumors examined to date have identifiable p53 gene point mutations or deletions. (4,5,6,7,14) While some p53 gene mutation is heritable, the majority of tumor suppressor gene mutation appears inducible, primarily by environmental factors. (8,9,11,12,13,15,16,17)

Although genetics undoubtedly play a role in susceptibility to cancer, it is estimated that less than 25% of all cancers are genetically related. (58)

2. 2.) Chronic viral infections. Chronic infections of Epstein-Barr(EBV) (18,19,20,21,32) ,Human Papilloma (HPV) (22,23,24,25), Hepatitis C (HCV) (26), Hepatitis B (HBV) (27), Cytomegalovirus (CMV) (28,29,30), human polyomaviruses JC(JCV) and BK (BKV) (31), and others predispose to cancer development.

3. 3.) Chronic inflammation.(32,33,34,35,36,37,38,39,40,41,42,43,44,47)

4. 4.) Toxins, both endogenous and exogenous, can initiate cancer by causing ROS which in turn damage DNA. A number of exogenous and endogenous chemicals are considered carcinogenic, although the rate and degree of internal detoxification, especially phase II liver enzymes, are an important part of the initiation process. Few substances are carcinogenic per se without contribution from faulty or under-functioning internal detoxification systems. (53,54,55,56,57,58,59)

5. 5.) Ionizing radiation. X-rays and other sources of ionizing radiation are known to cause DNA mutations consistent with cancer initiation. (60)

Cancer Promoters

DNA damage alone is usually insufficient to initiate tumor development. If the DNA damage is repaired or the damaged cell is eliminated, the multi-step process of cancer development will be thwarted. If, however, mutagenic damage is not repaired and/or the damaged cell is not eliminated, and if the cellular environment is conducive to cell growth, then damaged cells can multiply. This stage is known as “progression” and it is a necessary step for the development of malignancy. Factors which promote malignant cell growth include:

1.) Nutritional deficiencies. Certain vitamins, minerals, trace minerals and phytonutrients act in a number of ways to thwart malignant cell promotion. The mechanisms of actions are many and varied but include ROS inactivation, upregulation of detoxification pathways, esp. phase II liver enzyme pathways, direct decrease or neutralization of carcinogenic compounds, and immune system enhancement. Deficiencies of any one of the nutrients involved in these protective processes can leave the organism vulnerable to the promotion phase of cancer development.(61,62,63,64,65,66,67,68,69,70,71)

2.) Extracellular milieu. Blood glucose, insulin, cortisol, and arachadonic-derived prostatglandins (especially PGE2) act as promoters. In hormone-responsive cancers, estrogens, testosterone, prolactin and sex hormone metabolites and mimickers can also promote cell growth. The metabolic state of the organism therefore plays a major role in the promotion of cancer. (72,73,74,75,76,77)

3.) Inflammation. In addition to being an initiator of cancer, inflammation also acts to promote cancer in several ways, primarily by altering the cell-to-cell communication and delaying local detoxification. (32,33,34,35,37,38,39,40)

Treatment Strategies

Treatment strategies involve interfering with cancer progression at any phase of development, but initiation and promotion stages present the greatest opportunity for intervention.

To prevent the DNA damage which occurs during initiation, steps can be taken to mitigate sources of mutation, as follows:

I.) Genetic factors. While this aspect of initiation might seem the hardest to compensate for, it must be remembered that genetic mutation represents only weakness, not a forgone conclusion that cancer will develop. Minimizing other predispositions to initiation, such as nutrient deficiencies and carcinogenic exposure, can be sufficient to overcome heritable weaknesses. Further, dietary fasting, calorie restriction (CR) or a ketogenic diet (KD) have been shown to suppress the p53 oncogene, rendering this most common genetic factor less relevant. (78)

II.) Chronic viral infections. As with genetic factors, the presence of a chronic viral infection does not, by itself, mean an initiating certainly. Immune-enhancing strategies, anti-viral therapies and avoidance of other known initiators may be sufficient to prevent virally-caused mutagenesis.

III.) Chronic inflammation. Now known as a risk factor for heart disease, rheumatic disease and cancer, even subtle levels of inflammation, as measured by an hs-CRP blood test, can elevate risk of initiation. Fortunately, such inflammatory conditions respond well to nutritional, botanical and dietary modification. CR and KD have both been shown to reduce inflammation. Bromelain, curcumin and other anti-cancer drugs are, perhaps not coincidentally, also potent anti-inflammatory substances.

IV.) Toxins and radiation. Minimization of exposure and optimal dietary antioxidants can help offset the effects of environmental toxins, whether chemicals or ionizing radiation. Avoidance of exposure is also an obvious but often-overlooked preventive measure.

The Most Potent Anti-Cancer Strategy Known

“Attack by stratagem: hence, to fight and conquer in all your battles is not supreme excellence; supreme excellence consists in breaking the enemy’s resistance without fighting” —Sun Tzu, “The Art of War”

Nutritional and botanical factors can have profound positive effects in cancer treatment, either alone or as adjuncts to conventional treatment.

The single most potent anti-cancer strategy documented in the medical literature is to strike at the core of cancer’s metabolism: anaerobic glycolysis. Numerous animal and human studies have demonstrated that the glycolytic pathway of cancer cells can be confounded by the metabolic state of ketosis, often with profound apoptotic effects on cancer cells but without consequence to normal cells. In fact, the metabolic state of ketosis may curtail cancer growth by a number of different mechanisms:

I.) Greatly decreasing the glucose substrate required for cancer cell metabolism. Most tumors express abnormalities in the number and function of their mitochondria (80,81,88,89). Such abnormalities would prevent the bioenergetic utilization of ketone bodies, which require functional mitochondria for their oxidation.

II.) Decreasing insulin, a secondary growth factor for cancer cells.

III.) Decreasing inflammation (metabolic ketosis has anti-inflammatory effects). (85,86,87)

IV.) Decreasing ROS production. (82,83,84)

As one author pointed out, why would we believe that cells damaged by mutation are more resilient than normal cells? The answer is: they are not. Malignant cells are largely incapable of the metabolic flexibility displayed by normal cells, and therein lies their weakness and the potential for a gentle but highly effective point of attack.

Ketosis can be achieved by a high fat, moderate protein, low carbohydrate diet or by a calorie-restricted (CR) diet. Both methods of achieving ketosis have proven to decrease the production of ROS. Calorie restriction (CR) has a long history of experimentation in animals where it has also been seen to increase ROS antioxidant defense systems including superoxide dismutase, catalase, and glutathione peroxidase. (90)

In spite of improved availability of foods containing anti-carcinogenic phytonutrients and vitamins, many types of cancer have not declined as expected. This correlates to the overall calorie increase and overweight condition of our society, a condition which puts us in “constant feast” mode instead of the periodic fasting our ancestors previously experienced. (91) Many observers feel that our previous occasional fast, which would induce ketosis, was also beneficial for cancer control. It has also been hypothesized that some alternative cancer treatments, such as juice fasting or the use of Coley’s toxins, are effective primarily because they induce metabolic ketosis.

Additional Nutritional and Botanical Interventions

Although virtually any nutrient or herb can be considered in cancer treatment because of the multiple systems involved in same, only a relatively small handful of specific nutrients and botanicals have been well-studied and consistently proven to benefit the cancer patient. We will confine our discussion to those substances with a long history of use in human malignancy.

Nutritional Supplementation in the Treatment of Cancer

Supplements of proven utility in cancer treatment include:

I.) Vitamin C: long used for it’s dual function of immune up-regulation and direct toxicity to cancer cells, but doses sufficient to achieve the cytotoxic effect are unobtainable via the oral route. For this reason, IV vitamin C should be considered in cancer therapy. (92)

II.) Vitamin D3 (cholecalciferol): vitamin D deficiency is a known risk factor for cancer development.(93) D3 induces differentiation, inhibits angiogenesis (94, 95,96) and shows antitumor activity.(97,98,99) It may also up-regulate vitamin A receptors.(94) Vitamin D3 may serve to prevent metastatic bone disease in higher doses, perhaps because it is needed for normal calcification of bone matrix.

III.) Melatonin: a hormone produced by the pituitary gland which regulates sleep and circadian rhythms. Melatonin is a more potent antioxidant than glutathione or vitamin E (101). In vitro, it demonstrates anti-estrogen activity and immune stimulation. (100) Recent studies show that melatonin inhibits cell proliferation profoundly in vivo but only weakly in vitro. It is synergistic with IL-2 and increases the effectiveness of IL-2 treatment. (102)

IV.) CoQ10 (ubiquinone): this vitamin-like compound is involved in mitochondrial energy production. The heart is a high user of CoQ10 and many chemotherapeutic drugs deplete body stores of this nutrient. CoQ10 has been used successfully to reduce chemotherapy-induced cardio toxicity. In breast cancer patients, a dose of 90mg daily increases late stage survival dramatically. Three cases of complete remission have been documented at higher doses (300-400mg) per day. (103)

V.) Selenium: studies show that seleium interferes with the activity of p53 genes that promote the growth of cancer and induces apoptosis (104,105,106).

VI.) Tocotrienols: a member of the Vitamin E family, tocotrienols induce apoptosis and S-phase arrest (107,108) and inhibit proliferation. (109)

Botanical Considerations in Cancer Treatment

A HIGHLY SELECTIVE MATERIA MEDICA

Classified by action:

Natural Killer (NK) Cell Activation

Allium sativum

Astragalus

Echinacea spp.

Eleutherococcus senticosus

Panax ginseng

T-Cell Activation

Allium sativum

Astragalus

Echinacea spp.

Eleutherococcus

Anti-tumerogenic

Allium sativum

Berberine derivatives:

Hydrastis canadensis

Berberis aquifolia

B. vulgaris

Curcuma longa

Echinacea spp.

Stimulants of IgG & IgM Production

Panax ginseng

Anti-inflammatory

Ananas comosus

Curcuma longa

Fibrinolytic

Allium sativum

Ananas comosus

Macrophage Activation

Allium sativum

Aloe vera

Berberine derivatives:

Hydrastis canadensis

Berberis aquafolia

B. vulgaris

Coumarine derivatives:

Angelica sinensis-dong quai

Meliotus officinalis-sweet clover

Trifolium pratense- red clover

Echinacea spp.

Anti-metastatic

Ananas comosus

Larix spp.

modified citrus pectin (MCP)

Cytotoxic (IV administration)

Catharanthus roseus- periwinkle

vinblastin,vincristine,

vindesin,vinorelbine

Podophyllum peltatum-mayapple-podophyllotoxin

Taxus batacca- English yew- docetaxel

Taxotere®

Taxus brevifolia- Pacific yew- paclitaxel

Taxol®

Viscum album-mistletoe- Iscador®]

Materia Medica

Allium sativum (Liliaceae) – Garlic

As a food and a medicine, garlic comes closest to being a true panacea. Research has proved garlic’s immune-potentiating ability, including activation of NK and T-cells. (1,2,3,4.) Garlic is fibrinolytic, decreases platelet aggragation (5,6,7) and has been shown to have direct anti-tumor effects. 8,9,10. It is also a potent broad-spectrum antimicrobial, effective against alpha- and beta- Strep., E. coli., Klebsiella pneumonia, Mycobacterium, Salmonella, Staph. aureus, and Proteus spp. (17, 18, 19)

Aloe vera (Liliaceae) – Aloes

Acemannan, a water-soluable polysaccharide in Aloe vera, is a known immuno-stimulant (27,28) and anti-viral. (29) It’s mechanism of action is thought to be via stimulation of macrophage secretion of Tumor Necrosis Factor (TNF), interleukon, and interferon.

Ananas comosus (Bromeliaceae) – Pineapple (bromelain)

Bromelain is a sulfur-containing proteolytic enzyme from the stem of the pineapple plant. Other constituents include a non-proteolytic plasminogen activator, a peroxidase, and several protease inhibitors. (22,23)

Bromelain possesses significant anti-inflammatory activity by selective inhibition of pro-inflammatory prostaglandins. (16, 20) It also possesses fibrinolytic activity secondary to plasminogen activator (21) which may account for the antimetastatic properties seen in vivo. (24, 25, 26)

Astragalus membranaceus (Leguminosae) – Astragalus, Milk Vetch, Huang QI

Astragalus increases NK and T cell activity (11,12) in both normal and immunocompromised hosts.(13) It increases interferon production and is antibiotic against Shigella, Strep., Staph. and Diplococcus.(15)

Berberine derivatives:

Hydrastis Canadensis – (Ranunculaceae) – Goldenseal

Berberis aquafolia – (Berberidaceae) – Oregon Grape

Berberis vulgaris – (Berberidaceae) – Barberry

Berberine, an alkaloid derivative from various plants, has demonstrated significant antitumor effects with kill rates of 81% in vivo and 91% in vitro. This compares favorably to BCNU, a chemotherapeutic agent with a kill rate of 43% in vitro. (30)

Berberine sulfate also shows macrophage activation and cytostatic activity against tumor cells in vitro. (31) Berberine is well known for its broad spectrum antimicrobial activity (32,33,34) which is most effective in a neutral to alkaline medium. (35)

Courmarin derivatives:

Angelica sinensis – (Umbelliferaceae) – Dong quai

Metolium officinalis – Sweet clover

Trifolium pretense – (Leguminosae) – Red clover

Coumarin (1,2-benzopyrone) is a component of several medicinal plants that have been used historically in the treatment of cancer. Recent research has shown an immunomodulatory effect through activation of macrophages and monocytes. (39)

Curcuma longa – (Zingiberaceae) – Turmeric

Curcumin, a major component in turmeric, is a potent antioxidant and hepatoprotectant. It has been shown to inhibit cancer in all stages of development (initiation, promotion, and progression), (36) and provide symptom relief when used topically on external cancers. (37)

Anti-inflammatory effects are believed due to its ability stabilize lysosomal membranes and uncouple oxidative phosphorylation. At higher doses, curcumin stimulates endogenous corticoid release. (38)

Echinacea purpura, E. angustifolia (Compositae) – Purple coneflower

Echinacea is one of the most widely studied medicinal herbs, and its immune-potentiating effects are not in question.

Arabinogalactin, a purified polysaccharide from E. purpura, has been shown to activate macrophage cytotoxicity to tumor cells, increase interferon production, stimulate T-lymphocyte production and activity, enhance NK cell activity and increase levels of circulating neutrophils. (40, 41, 42,43)

Echinacea stimulates non-specific defense mechanisms including alternate complement pathway. (44) It is anti-tumerogenic in animal models. (45)

Eleutherococcus senticosis – (Araliaceae) – Siberian ginseng

Eleutherococcus has been shown to both elevate numbers and activate helper / inducer lymphocytes and NK cells. (46)

It has been revered in Russia as an adaptogen, and studies confirm that it normalizes numerous physical functions regardless of the direction of imbalance. (47)

Larix occidentalis, L. dahurica – (Pinaceae) – Larch

Larch is a deciduous conifer that contains an arabinogalactan similar to that in other “immune enhancing” herbs including Echinacea spp., Baptisia tinctora, and Curcuma longa.

Larch arabinogalactans have been shown to reduce the number of liver metastasis in multiple studies (48,49,50,51), perhaps by acting as a “reverse lectin” and blocking tumor binding sites. (52) A similar effect has been noted for Modified Citrus Pectin (MCP). (See below)

Panax ginseng – (Araliaceae) – Chinese or Korean ginseng

Ginsenosides, an active constituent in P. ginseng, have been shown to increase both the number and the activity of lymphocytes in healthy subjects. (53)

Large doses in lab animals (human equivalent of 500 -125,000 mg) for five days increased IgG and IgM formation by 50 and 100% respectively, and enhanced NK cell activity and interferon production. (54)

Ginseng has long been considered an adaptogenic herb, and recent research verifies that it increases resistance to physical and chemical stress. (55,56)

Modified Citrus Pectin (MCP)

Pectin, a high molecular-weight polysaccharide present in the cell wall of all plants, can be pH degraded to produce a modified (smaller) polysaccharide with anti-metastatic capabilities. (57) MCP appears to bind with galectins on cancer cell surfaces, inhibiting aggregation and adherence to normal cells (58) and offering anti-metastatic protection in animal models. (59,60,61)

In Summary

Much more is known about the management of cancer, including how to evoke durable remissions and even cure, than is generally used or discussed in conventional medicine. Perhaps this is because some of the most powerful and proven therapies do not require drugs or invasive intervention.

“Those who battle nature as their enemy will lose; those who use nature to battle their enemy will win.” —Mark Ziemann, R.N.

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Natural Strategies And Support

What if you’ve already been diagnosed with cancer? The first thing to remember is — don’t panic. Cancer is not a death sentence. Many good treatments for cancer exist. A few are found in conventional medicine. Many others are available in natural, alternative and “unconventional” medicine. Non-toxic treatments for cancer have been used successfully by many people, with and without conventional treatment.

If you are going to use alternative treatments, OR if you decide to integrate natural and alternative treatments with conventional care, it is best to seek the help of a qualified “integrative” practitioner. (Someone like myself who uses all avenues of medicine, from conventional to natural, with the foremost regard for the patient’s welfare — not the type of treatment used).

The type of cancer, it’s location, the age and health of the patient, all make a difference as to what the best course of action will be. For example, juice fasting has helped some people but should be strictly avoided by others. Certain medications and surgeries are helpful in some types of cancer, useless in others.

All of these questions need to be answered with the assistance of an holistic physician who can help you determine the best course of action to take and will work with you to sort out the legitimate treatments from the “hype.” There is no room for guesswork and inexperience once a diagnosis of cancer has been made. (Please, consider obtaining a consultation with Dr. Myatt).

DIET AND LIFESTYLE RECOMMENDATIONS

• Eat a low carbohydrate diet with as much organically-produced food as possible. (The primary “fuel” of cancer cells is glucose, or sugar).  Include plenty of “Super Foods,” especially fresh garlic. Do NOT juice fast or undergo other radical diets until you have conferred with an holistic physician.
• Drink 64 ounces of pure water daily.
• Exercise moderately if you are able. Walking is one of the best. Your holistic physician can work with you to design an optimal exercise program.
• Attend a support group. Studies have shown that people fare better with cancer when they attend such support groups.
• Stop negative health habits immediately! This includes smoking or other tobacco use and alcohol.
• Practice meditation, relaxation, prayer or your chosen form of spiritually-directed activity.

PRIMARY SUPPORT

• • • Maxi Multi: 3 caps, 3 times per day with meals. Optimal (not minimal) doses of antioxidants (ACES), are particularly important. Many nutrients help prevent side effects from chemotherapy and radiation, but be sure to check with your holistic physician to insure that there are no unwanted interactions with various chemotherapy medications.
  • • Omega 3 fatty acids:
      Flax seed meal, 2 teaspoons per day with food
      OR
      Flax seed capsules: 2-4 caps, 3 times per day (target dose range: 6-12 caps per day)
      OR
      Flax seed oil: 1 tablespoon per day
      OR
      Max EPA (Omega-3 rich fish oil): 1-2 caps, 3 times per day with meals (target dose: 3-6 caps per day).
  • • CoQ10: 50-300mg per day. This powerful antioxidant, produced by the body, diminishes with age. It is especially valuable for all types of heart disease. CHOLESTEROL-LOWERING DRUGS deplete CoQ10.
  • • Vitamin C: take an additional 3,000-10,000mg per day in divided doses. Some studies show that IV vitamin C may be more effective.
  • • Grape Seed Extract (resveretrol): 2 caps, 2-3 times daily with meals
  • • Turmeric: 1-2 caps, 3 times per day with meals
  • • Vitamin D: 1,000-5,000IU per day based on blood test results
  • • Bromelain: 1-2 caps, 3 times per day between meals
    • Melatonin: 3-20mg at bedtime (DO NOT use in lymphoma or melanoma)ADDITIONAL SUPPORT

      For Breast Cancer

       

    • Calcium D-glucarate: 2-3 caps, 3 times per day with meals or as directed.
    • Diindolymethane (DIM): 2 caps, 2 times per day.
      For Prostate Cancer

       

    • Lycopene: (15mg): 1 capsule per day with a meal.

 

For all cancers (anti-metastatic)

• • • • Larch arabinogalactin: 2-3 caps, 3 times per day
        OR
      • Modified Citrus Pectin: 2 caps, 3 times per day or as directed by your health care practitioner.

Note: If you have been diagnosed with cancer and want to explore your options, it is most important to seek qualified help. DO NOT rely on second-hand stories from well-meaning friends and family members. Good treatments, and combinations of treatments, exist for many types of cancers, but relying on anecdotal stories and unproven “remedies” can be a waste of time and money. More importantly, unproven treatments can lead you away from legitimately helpful treatments.

 

Dr. Myatt is available for consultations by telephone. She does extensive research and teaching in the field of both conventional cancer treatment and alternative therapies.

---

References

Low Carbohydrate Diet

1.) Freedland SJ, Mavropoulos J, Wang A, Darshan M, Demark-Wahnefried W, Aronson WJ, Cohen P, Hwang D, Peterson B, Fields T, Pizzo SV, Isaacs WB. Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. Prostate. 2008 Jan 1;68(1):11-9.
2.) Venkateswaran V, Haddad AQ, Fleshner NE, Fan R, Sugar LM, Nam R, Klotz LH, Pollak M. Association of diet-induced hyperinsulinemia with accelerated growth of prostate cancer (LNCaP) xenografts.J Natl Cancer Inst. 2007 Dec 5;99(23):1793-800. Epub 2007 Nov 27.
3.) Zhou W, Mukherjee P, Kiebish MA, Markis WT, Mantis JG, Seyfried TN. The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer.Nutr Metab (Lond). 2007 Feb 21;4:5.
4.) Borugian MJ, Sheps SB, Kim-Sing C, Van Patten C, Potter JD, Dunn B, Gallagher RP, Hislop TG. Insulin, macronutrient intake, and physical activity: are potential indicators of insulin resistance associated with mortality from breast cancer? Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1163-72.
5.) Seyfried TN, Sanderson TM, El-Abbadi MM, McGowan R, Mukherjee P.: Role of glucose and ketone bodies in the metabolic control of experimental brain cancer.Br J Cancer. 2003 Oct 6;89(7):1375-82.
6.) Muti P, Quattrin T, Grant BJ, Krogh V, Micheli A, Schünemann HJ, Ram M, Freudenheim JL, Sieri S, Trevisan M, Berrino F. Fasting glucose is a risk factor for breast cancer: a prospective study. Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1361-8.
7.) Meixensberger J, Herting B, Roggendorf W, Reichmann H: Metabolic patterns in malignant gliomas.J Neurooncol 1995, 24:153-161
8.) Fearon KC.: Nutritional pharmacology in the treatment of neoplastic disease.Baillieres Clin Gastroenterol. 1988 Oct;2(4):941-9.
9.) Pedersen PL: Tumor mitochondria and the bioenergetics of cancer cells. Prog Exp Tumor Res 1978, 22:190-274.

Garlic

1.) Morioka, N., Morton, D.L., and Irie, R.F.: A protein fraction from aged garlic extract enhances cytotoxicity and proliferation of human lymphocytes mediated by interleukin-2 and conavalin. Proc Ann Meet Am Assoc Cancer 34:A3297, 1993.
2.) Legnani C., Frascaro M., Guazzaloca G., et al.: Effects of a dried garlic preparation on fibrinolysis and platelet aggragation in healthy subjects. Arzneim Forsch Drug Res 43:119-122, 1993.
3.) Kiesewetter H., et al.: effects of garlic coated tablets in peripheral arterial occlusive disease. Clin Investig 71:383-86, 1993.
4.) Lau, B.H., Yamasaki, T., and Gridley, D.S.: Garlic compounds modulate macrophage and T-lymphocyte function. Mol Biother 3:103-107, 1991.
5.) Dausch JG., Nixon DW.: Garlic: a review of its relationship to malignant disease. Prev Med 19:346-61, 1990.
6.) Kandil O.M., et al.: Garlic and the immune system in humans: its effect on natural killer cells. Fed Proc 46:441, 1987.
7.) Kandil, O.M. et. al.: Garlic and the immune system in humans: Its effect on natural killer cells. Fed Proc 46:441, 1987.
8.) Belman S.: Onion and garlic oils prohibit tumor promotion. Carcinogenesis 4(8):1063-5, 1983.
9.) Kroning, F.: Garlic as an inhibitor for spontaneous tumors in predisposed mice. Acta Unio Inter Contra Cancrum 20(3):855, 1964.

Super Foods

1.) Khan N, Afaq F, Mukhtar H. Cancer Chemoprevention Through Dietary Antioxidants: Progress and Promise. Antioxid Redox Signal. 2007 Dec 21 [Epub ahead of print].
2.) Moreno DA, López-Berenguer C, García-Viguera C. Effects of stir-fry cooking with different edible oils on the phytochemical composition of broccoli. J Food Sci. 2007 Jan;72(1):S064-8.

Exercise and Cancer

1.) Valenti M, Porzio G, Aielli F, Verna L, Cannita K, Manno R, Masedu F, Marchetti P, Ficorella C.Physical exercise and quality of life in breast cancer survivors. Int J Med Sci. 2008 Jan 15;5(1):24-8.
2.) Greenspan SL. Approach to the prostate cancer patient with bone disease. J Clin Endocrinol Metab. 2008 Jan;93(1):2-7.
3.) Farrell SW, Cortese GM, Lamonte MJ, Blair SN.Cardiorespiratory fitness, different measures of adiposity, and cancer mortality in men.Obesity (Silver Spring). 2007 Dec;15(12):3140-9.
4.) McBride D. Healthful eating and exercise may lower  mortality after breast cancer. ONS Connect. 2007 Dec;22(12):27.
5.) Karvinen KH, Courneya KS, North S, Venner P.  Associations between exercise and quality of life in bladder cancer survivors: a population-based study.Cancer Epidemiol Biomarkers Prev. 2007 May;16(5):984-90.
6.) Kruk J. Physical activity in the prevention of the most frequent chronic diseases: an analysis of the recent evidence. Asian Pac J Cancer Prev. 2007 Jul-Sep;8(3):325-38.
7.) Lynch BM, Cerin E, Owen N, Aitken JF. Associations of leisure-time physical activity with quality of life in a large, population-based sample of colorectal cancer survivors. Cancer Causes Control. 2007 Sep;18(7):735-42. Epub 2007 May 23.
8.) Milne HM, Gordon S, Guilfoyle A, Wallman KE, Courneya KS. Association between physical activity and quality of life among Western Australian breast cancer survivors. Psychooncology. 2007 Dec;16(12):1059-68.
9.) Stevinson C, Faught W, Steed H, Tonkin K, Ladha AB, Vallance JK, Capstick V, Schepansky A, Courneya KS.Associations between physical activity and quality of life in ovarian cancer survivors. Gynecol Oncol. 2007 Jul;106(1):244-50. Epub 2007 May 9.
10.) Chang SC, Ziegler RG, Dunn B, Stolzenberg-Solomon R, Lacey JV Jr, Huang WY, Schatzkin A, Reding D, Hoover RN, Hartge P, Leitzmann MF. Association of energy intake and energy balance with postmenopausal breast cancer in the prostate, lung, colorectal, and ovarian cancer screening trial. Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):334-41.
11.) Rogers LQ, Courneya KS, Robbins KT, Malone J, Seiz A, Koch L, Rao K, Nagarkar M. Physical activity and quality of life in head and neck cancer survivors. 1: Support Care Cancer. 2006 Oct;14(10):1012-9. Epub 2006 Mar 15.
12.) Hanna L, Adams M. Prevention of ovarian cancer. Best Pract Res Clin Obstet Gynaecol. 2006 Apr;20(2):339-62. Epub 2005 Dec 20.
13.) Pan SY, Ugnat AM, Mao Y. Physical activity and the risk of ovarian cancer: a case-control study in Canada. Int J Cancer. 2005 Nov 1;117(2):300-7.
14.) Courneya KS, Karvinen KH, Campbell KL, Pearcey RG,  Dundas G, Capstick V, Tonkin KS. Associations among exercise, body weight, and quality of life in a population-based sample of endometrial cancer survivors. Gynecol Oncol. 2005 May;97(2):422-30.
15.) Vallance JK, Courneya KS, Jones LW, Reiman T. Differences in quality of life between non-Hodgkin’s lymphoma survivors meeting and not meeting public health exercise guidelines. Psychooncology. 2005 Nov;14(11):979-91.
16.) Zhang M, Xie X, Lee AH, Binns CW.Sedentary behaviours and epithelial ovarian cancer risk. Cancer Causes Control. 2004 Feb;15(1):83-9.

Support Groups

1.) Gottlieb BH, Wachala ED. Cancer support groups: a critical review of empirical studies. Psychooncology. 2007 May;16(5):379-400.
2.) Goodwin PJ. Support groups in advanced breast cancer. Cancer. 2005 Dec 1;104(11 Suppl):2596-601.
3.) Cunningham AJ, Watson K. How psychological therapy may prolong survival in cancer patients: new evidence and a simple theory. Integr Cancer Ther. 2004 Sep;3(3):214-29.
4.) Cunningham AJ, Phillips C, Stephen J, Edmonds C. Fighting for life: a qualitative analysis of the process of psychotherapy-assisted self-help in patients with metastatic cancer. Integr Cancer Ther. 2002 Jun;1(2):146-61.

Stop Tobacco and Alcohol Use

1.) Kaufman EL, Jacobson JS, Hershman DL, Desai M, Neugut AI. Effect of breast cancer radiotherapy and cigarette smoking on risk of second primary lung cancer. J Clin Oncol. 2008 Jan 20;26(3):392-8.
2.) Park SM, Lim MK, Jung KW, Shin SA, Yoo KY, Yun YH, Huh BY. Prediagnosis smoking, obesity, insulin resistance, and second primary cancer risk in male cancer survivors: National Health Insurance Corporation Study. J Clin Oncol. 2007 Oct 20;25(30):4835-43.
3.) Koskinen WJ, Brøndbo K, Mellin Dahlstrand H, Luostarinen T, Hakulinen T, Leivo I, Molijn A, Quint WG, Røysland T, Munck-Wikland E, Mäkitie AA, Pyykkö I, Dillner J, Vaheri A,
Aaltonen LM. Alcohol, smoking and human papillomavirus in laryngeal carcinoma: a Nordic prospective multicenter study. J Cancer Res Clin Oncol. 2007 Sep;133(9):673-8. Epub 2007 May 8.
4.) Muwonge R, Ramadas K, Sankila R, Thara S, Thomas G, Vinoda J, Sankaranarayanan R. Role of tobacco smoking, chewing and alcohol drinking in the risk of oral cancer in Trivandrum, India: A nested case-control design using incident cancer cases. Oral Oncol. 2007 Oct 12
5.) Chen CH, Shun CT, Huang KH, Huang CY, Tsai YC, Yu HJ, Pu YS. Stopping smoking might reduce tumour recurrence in nonmuscle-invasive bladder cancer. BJU Int. 2007 Aug;100(2):281-6; discussion 286. Epub 2007 Apr 5.
6.) Rieck G, Fiander A.The effect of lifestyle factors on gynaecological cancer. Best Pract Res Clin Obstet Gynaecol. 2006 Apr;20(2):227-51.
7.) Ford MB, Sigurdson AJ, Petrulis ES, Ng CS, Kemp B, Cooksley C, McNeese M, Selwyn BJ, Spitz MR, Bondy ML.Effects of smoking and radiotherapy on lung carcinoma in breast carcinoma
survivors. Cancer. 2003 Oct 1;98(7):1457-64.
8.) van Leeuwen FE, Klokman WJ, Stovall M, Hagenbeek A, van den Belt-Dusebout AW, Noyon R, Boice JD Jr, Burgers JM, Somers R. Roles of radiotherapy and smoking in lung cancer following Hodgkin’s disease. J Natl Cancer Inst. 1995 Oct 18;87(20):1530-7.
9.) Neugut AI, Murray T, Santos J, Amols H, Hayes MK, Flannery JT, Robinson E. Increased risk of lung cancer after breast cancer radiation therapy in cigarette smokers. Cancer. 1994 Mar
15;73(6):1541-3.
10.) Day GL, Blot WJ, Shore RE, McLaughlin JK, Austin DF, Greenberg RS, Liff JM, Preston-Martin S, Sarkar S, Schoenberg JB, et al. Second cancers following oral and pharyngeal cancers: role of tobacco and alcohol. J Natl Cancer Inst. 1994 Jan 19;86(2):131-7.
11.) Day GL, Shore RE, Blot WJ, McLaughlin JK, Austin DF, Greenberg RS, Liff JM, Preston-Martin S, Sarkar S, Schoenberg JB, et al. Dietary factors and second primary cancers: a follow-up of oral and pharyngeal cancer patients. Nutr Cancer. 1994;21(3):223-32.

Meditation, Relaxation, Prayer

1.) Cunningham AJ, Phillips C, Lockwood GA, Hedley DW, Edmonds CV. Association of involvement in psychological self-regulation with longer survival in patients with metastatic
cancer: an exploratory study. Adv Mind Body Med. 2000 Fall;16(4):276-87.
2.) Greer S. Improving quality of life: adjuvant psychological therapy for patients with cancer. Support Care Cancer. 1995 Jul;3(4):248-51.

Multiple Vitamins and Cancer

1.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival,
part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival,
Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
3.) Tsao SM, Yin MC, Liu WH. Oxidant stress and B vitamins status in patients with non-small cell lung cancer. Nutr Cancer. 2007;59(1):8-13.
4.) Moss RW. Should patients undergoing chemotherapy and radiotherapy be prescribed antioxidants? Integr Cancer Ther. 2006 Mar;5(1):63-82.
5.) Moyad MA. The use of complementary/preventive medicine to prevent prostate cancer recurrence/progression following definitive therapy. Part II–rapid review of dietary supplements.
Curr Opin Urol. 2003 Mar;13(2):147-51.
6.) Moyad MA. Potential lifestyle and dietary supplement options for the prevention and postdiagnosis of bladder cancer. Urol Clin North Am. 2002 Feb;29(1):31-48, viii.
7.) Kamat AM, Lamm DL. Diet and nutrition in urologic cancer. W V Med J. 2000 May-Jun;96(3):449-54.
9.) Jatoi A, Daly BD, Kramer G, Mason JB. A cross-sectional study of vitamin intake in postoperative non-small cell lung cancer patients. J Surg Oncol 1998;68:231–6.
10.) Jatoi A, Daly BD, Kramer G, Mason JB. A cross-sectional study of vitamin intake in postoperative non-small cell lung cancer patients. J Surg Oncol 1998;68:231–6.
11.) Lamm DL, Riggs DR, Shriver JS, vanGilder PF, Rach JF, DeHaven JI. Megadose vitamins in bladder cancer: a double-blind clinical trial. J Urol. 1994 Jan;151(1):21-6.

Antioxidants (General) and Cancer

1.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
3.) Kirsh VA, Hayes RB, Mayne ST, Chatterjee N, Subar AF, Dixon LB, Albanes D, Andriole GL, Urban DA, Peters U; PLCO Trial. Supplemental and dietary vitamin E, beta-carotene, and vitamin C intakes and prostate cancer risk.J Natl Cancer Inst. 2006 Feb 15;98(4):245-54.
4.) Berger MM. Can oxidative damage be treated nutritionally? Clin Nutr. 2005 Apr;24(2):172-83.
5.) Ferguson LR, Philpott M, Karunasinghe N. Dietary cancer and prevention using antimutagens. Toxicology. 2004 May 20;198(1-3):147-59.
6.) Borek C. Dietary antioxidants and human cancer.Integr Cancer Ther. 2004 Dec;3(4):333-41.
7.) Prasad KN. Multiple dietary antioxidants enhance the efficacy of standard and experimental cancer therapies and decrease their toxicity. Integr Cancer Ther. 2004 Dec;3(4):310-22.
8.) Heyland DK, Dhaliwal R, Suchner U, Berger MM. Antioxidant nutrients: a systematic review of trace elements and vitamins in the critically ill patient. Intensive Care Med. 2005 Mar;31(3):327-37. Epub 2004 Dec 17.
9.) Kim YT, Kim JW, Choi JS, Kim SH, Choi EK, Cho NH. Relation between deranged antioxidant system and cervical neoplasia. Int J Gynecol Cancer. 2004 Sep-Oct;14(5):889-95.
10.) Drisko JA, Chapman J, Hunter VJ. The use of antioxidant therapies during chemotherapy. Gynecol Oncol. 2003 Mar;88(3):434-9.
11.) Prasad KN, Cole WC, Kumar B, Prasad KC. Scientific rationale for using high-dose multiple micronutrients as an adjunct to standard and experimental cancer therapies. J Am Coll Nutr. 2001 Oct;20(5Suppl):450S-463S; discussion 473S-475S.
12.) Lamson DW, Brignall MS. Antioxidants in cancer therapy; their actions and interactions with oncologic therapies. Altern Med Rev. 1999 Oct;4(5):304-29.
13.) Prasad KN, Kumar A, Kochupillai V, Cole WC. High doses of multiple antioxidant vitamins: essential ingredients in improving the efficacy of standard cancer therapy. J Am Coll Nutr. 1999
Feb;18(1):13-25.
14.) Lupulescu A. The role of vitamins A, beta-carotene, E and C in cancer cell biology. Int J Vitam Nutr Res. 1994;64(1):3-14.
15.) Stähelin HB. Critical reappraisal of vitamins and trace minerals in nutritional support of cancer patients. Support Care Cancer. 1993 Nov;1(6):295-7.

Vitamin A and Carotenes

1.) Yuan JM, Ross RK, Gao YT, Qu YH, Chu XD, Yu MC. Prediagnostic levels of serum micronutrients in relation to risk of gastric cancer in Shanghai, China. Cancer Epidemiol Biomarkers Prev. 2004 Nov;13(11 Pt 1):1772-80.
2.) Wu K, Erdman JW Jr, Schwartz SJ, Platz EA, Leitzmann M, Clinton SK, DeGroff V, Willett WC, Giovannucci E.Plasma and dietary carotenoids, and the risk of prostate cancer: a nested case-control study. Cancer Epidemiol Biomarkers Prev. 2004 Feb;13(2):260-9.
3.) Kamat AM, Lamm DL. Chemoprevention of bladder cancer. Urol Clin North Am. 2002 Feb;29(1):157-68.
4.) Sato R, Helzlsouer KJ, Alberg AJ, Hoffman SC, Norkus EP, Comstock GW. Prospective study of carotenoids, tocopherols, and retinoid concentrations and the risk of breast cancer. Cancer
Epidemiol Biomarkers Prev. 2002 May;11(5):451-7.
5.) Gann PH, Ma J, Giovannucci E, Willett W, Sacks FM, Hennekens CH,Stampfer MJ. Lower prostate cancer risk in men with elevated plasma lycopene levels: results of a prospective analysis. Cancer Res. 1999 Mar 15;59(6):1225-30.
6.) Giovannucci E, Ascherio A, Rimm EB, Stampfer MJ, Colditz GA, Willett WC. ake of carotenoids and retinol in relation to risk of prostate cancer. J Natl Cancer Inst. 1995 Dec 6;87(23):1767-76.
7.) Majewski S, Szmurlo A, Marczak M, Jablonska S, Bollag W.: Synergistic effect of retinoids and interferon alpha on tumor-induced angiogenesis: anti-angiogenic effect on HPV-harboring
tumor-cell lines.Int J Cancer. 1994 Apr 1;57(1):81-5.
8.) Pastorino U, Infante M, Maioli M, et al. Adjuvant treatment of stage I lung cancer with high-dose vitamin A. J Clin Oncol 1993;11:1216–22.

Vitamin C

1.) Wybieralska E, Koza M, Sroka J, Czyz J, Madeja Z. Ascorbic acid inhibits the migration of walker 256 carcinosarcoma cells. Cell Mol Biol Lett. 2008;13(1):103-11. Epub 2007 Oct 29.
2.) Hanck A. Vitamin C and cancer. Int J Vit Nutr Res 1983;(Suppl #24):87–104 [review].
3.) Murata A, Morishige F, Yamaguchi H. Prolongation of survival times of terminal cancer patients by administration of large doses of ascorbate. Int J Vit Nutr Res 1982;(Suppl #23):103–14.
4.) Bussey HJR, DeCosse JJ, Deschner EE, et al. A randomized trial of ascorbic acid in polyposis coli. Cancer 1982;50:1434–9.
5.) Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: reevaluation of prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA 1978;75:4538–42.
6.) Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA 1976;73:3685–9.

Selenium

1.) Li H, Stampfer MJ, Giovannucci EL, Morris JS, Willett WC, Gaziano JM, Ma J.A prospective study of plasma selenium levels and prostate cancer risk. J Natl Cancer Inst. 2004 May
5;96(9):696-703.
2.) Yu M-W, Horng I-S, Hsu K-H, et al. Plasma selenium levels and risk of hepatocellular carcinoma among men with chronic hepatitis virus infection. Am J Epidemiol 1999;150:367–74.
3.) Knekt P, Marniemi J, Teppo L, et al. Is low selenium status a risk factor for lung cancer? 1998 Nov 15;148(10):975-82.
4.) Scieszka M, Danch A, Machalski M, Drozdz M. Plasma selenium concentration in patients with stomach and colon cancer in the Upper Silesia. Neoplasma 1997;44:395–7.
5.) Toma S, Micheletti A, Giacchero A, et al. Selenium therapy in patients with precancerous and malignant oral cavity lesions: preliminary results.Cancer Detection Prev 1991;15:491–3.
6.) Knekt P, Aromaa A, Maatela J, et al. Serum selenium and subsequent risk of cancer among Finnish men and women. J Natl Cancer Inst 1990;82:864–8.
7.) Burney PGJ, Comstock GW, Morris JS. Serologic precursors of cancer: serum micronutrients and the subsequent risk of pancreatic cancer. Am J Clin Nutr 1989;49:895–900.
8.) Helzlsouer KJ, Comstock GW, Morris JS. Selenium, lycopene, alpha-tocopherol, ß-carotene, retinol, and subsequent bladder cancer. Cancer Res 1989;49:6144–8.
9.) Jaskiewicz K, Marasas WF, Rossouw JE, et al. Selenium and other mineral elements in populations at risk for esophageal cancer. Cancer 1988;62:2635–9.
10.) Medina D, Morrison DG. Current ideas on selenium as a  chemopreventative agent. Pathol Immunopathol Res 1988;7:187–99.
11.) Fex G, Pettersson B, Akesson B. Low plasma selenium as a risk factor for cancer death in middle-aged men. Nutr Cancer 1987;10:221–9.
12.) Medina D. Mechanisms of selenium inhibition of tumorigenesis. Adv Exp Med Biol 1986;206:465–72.
13.) Willett WC, Polk BF, Morris JS, et al. Prediagnostic serum Selenium and risk of cancer. Lancet 1983;42:130–4.
14.) Beisel WR. Single nutrients and immunity. Am J Clin Nutr 1982;35:417–68.
15.) Shamberger RJ, Rukoven E, Lonfield AK, et al. Antioxidants and cancer. Selenium in the blood of normals and cancer patients. J Natl Cancer Inst 1973;4:863–70.

Omega 3 Essential Fatty Acids

1.) Colomer R, Moreno-Nogueira JM, García-Luna PP, García-Peris P, García-de-Lorenzo A, Zarazaga A, Quecedo L, del Llano J, Usán L, Casimiro C. N-3 fatty acids, cancer and cachexia: a systematic review of the literature. Br J Nutr. 2007 May;97(5):823-31.
2.) Zhang W, Long Y, Zhang J, Wang C. Modulatory effects of EPA and DHA on proliferation and apoptosis of pancreatic cancer cells. J Huazhong Univ Sci Technolog Med Sci. 2007 Oct;27(5):547-50.
3.) Dauchy RT, Dauchy EM, Davidson LK, Krause JA, Lynch DT, Tirrell PC, Tirrell RP, Sauer LA, Van der Riet P, Blask DE. Inhibition of fatty acid transport and proliferative activity in tissue-isolated human squamous cell cancer xenografts perfused in situ with melatonin or eicosapentaenoic or conjugated linoleic acids. Comp Med. 2007 Aug;57(4):377-82.
4.) Chen J, Power KA, Mann J, Cheng A, Thompson LU. Flaxseed alone or in combination with tamoxifen inhibits MCF-7 breast tumor growth in ovariectomized athymic mice with high circulating levels of estrogen. Exp Biol Med (Maywood). 2007 Sep;232(8):1071-80.
5.) Kolar SS, Barhoumi R, Callaway ES, Fan YY, Wang N, Lupton JR, Chapkin RS. Synergy between docosahexaenoic acid and butyrate elicits p53-independent apoptosis via mitochondrial Ca(2+) accumulation in colonocytes. Am J Physiol Gastrointest Liver
Physiol. 2007 Nov;293(5):G935-43. Epub 2007 Aug 23.
6.) Kato T, Kolenic N, Pardini RS. Docosahexaenoic acid (DHA), a primary tumor suppressive omega-3 fatty acid, inhibits growth of colorectal cancer independent of p53 mutational status. Nutr Cancer. 2007;58(2):178-87.
7.) Espada CE, Berra MA, Martinez MJ, Eynard AR, Pasqualini ME. Effect of Chia oil (Salvia Hispanica) rich in omega-3 fatty acids on the eicosanoid release, apoptosis and T-lymphocyte tumor infiltration in a murine mammary gland adenocarcinoma. Prostaglandins Leukot Essent Fatty Acids. 2007 Jul;77(1):21-8. Epub 2007 Jul 6.
8.) Saarinen NM, Power K, Chen J, Thompson LU. Flaxseed attenuates the tumor growth stimulating effect of soy protein in ovariectomized athymic mice with MCF-7 human breast cancer xenografts. Int J Cancer. 2006 Aug 15;119(4):925-31.
9.) Shirota T, Haji S, Yamasaki M, Iwasaki T, Hidaka T, Takeyama Y, Shiozaki H, Ohyanagi H. Apoptosis in human pancreatic cancer cells induced by eicosapentaenoic acid. Nutrition. 2005
Oct;21(10):1010-7.
10.) Schley PD, Jijon HB, Robinson LE, Field CJ. Mechanisms of omega-3 fatty acid-induced growth inhibition in MDA-MB-231 human breast cancer cells. Breast Cancer Res Treat. 2005
July;92(2):187-95.
11.) de Deckere EA. Possible beneficial effect of fish and fish n-3 polyunsaturated fatty acids in breast and colorectal cancer. Eur J Cancer Prev. 1999 Jul;8(3):213-21.
12.) Chang WL, Chapkin RS, Lupton JR. Fish oil blocks azoxymethane-induced rat colon tumorigenesis by increasing cell differentiation and apoptosis rather than decreasing cell
proliferation. J Nutr. 1998 Mar;128(3):491-7.
13.) Bagga D, Capone S, Wang HJ, Heber D, Lill M, Chap L, Glaspy JA. Dietary modulation of omega-3/omega-6 polyunsaturated fatty acid ratios in patients with breast cancer. J Natl Cancer Inst. 1997 Aug 6;89(15):1123-31.

CoQ10

1.) Caso G, Kelly P, McNurlan MA, Lawson WE. Effect of coenzyme q10 on myopathic symptoms in patients treated with statins. Am JCardiol. 2007 May 15;99(10):1409-12. Epub 2007 Apr 3.
2.) Premkumar VG, Yuvaraj S, Vijayasarathy K, Gangadaran SG, Sachdanandam P. Effect of coenzyme Q10, riboflavin and niacin onserum CEA and CA 15-3 levels in breast cancer patients undergoing tamoxifen therapy. Biol Pharm Bull. 2007 Feb;30(2):367-70.
3.) Premkumar VG, Yuvaraj S, Vijayasarathy K, Gangadaran SG, Sachdanandam P. Serum cytokine levels of interleukin-1beta, -6, -8,tumour necrosis factor-alpha and vascular endothelial growth factor in breast cancer patients treated with tamoxifen and supplemented with co-enzyme Q(10), riboflavin and niacin. Basic Clin Pharmacol Toxicol. 2007 Jun;100(6):387-91.
4.)  Rusciani L, Proietti I, Paradisi A, Rusciani A, Guerriero G, Mammone A, De Gaetano A, Lippa S. Recombinant interferon alpha-2b and coenzyme Q10 as a postsurgical adjuvant therapy for melanoma: a 3-year trial with recombinant interferon-alpha and 5-year
follow-up. Melanoma Res. 2007 Jun;17(3):177-83.
5.)  Rusciani L, Proietti I, Rusciani A, Paradisi A, Sbordoni G, Alfano C, Panunzi S, De Gaetano A, Lippa S. Low plasma coenzyme Q10 levels as an independent prognostic factor for melanoma progression. J Am Acad Dermatol. 2006 Feb;54(2):234-41.
6.)  Langsjoen PH, Langsjoen JO, Langsjoen AM, Lucas LA. Treatment of statin adverse effects with supplemental Coenzyme Q10 and statin drug discontinuation. Biofactors. 2005;25(1-4):147-52.
7.) Forgionne GA. Bovine cartilage, coenzyme Q10, and wheat grass therapy for primary peritoneal cancer. J Altern Complement Med. 2005 Feb;11(1):161-5.
8.) Silver MA, Langsjoen PH, Szabo S, Patil H, Zelinger A. Effect of atorvastatin on left ventricular diastolic function and ability of coenzyme Q10 to reverse that dysfunction. Am J Cardiol. 2004 Nov 15;94(10):1306-10.
9.)  Judy WV. Nutritional intervention in cancer prevention and treatment. American College for Advancement in Medicine Spring Conference, Ft. Lauderdale, FL. May 3, 1998.
10.) Boik, John: Cancer and Natural Medicine, Oregon Medical Press, 1995,p.71.
11.)  Lockwood K, Moesgaard S, Folkers K. Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10. Biochem Biophys Res Commun 1994;199:1504–8.
12.) Lockwood K, Moesgaard S, Yamamoto T, Folkers K. Progress on therapy of breast cancer with vitamin Q10 and the regression of metastases. Biochem Biophys Res Commun 1995;212:172–7.
13.)  Lockwood K, Moesgaard S, Hanioka T, Folkers K. Apparent partial remission of breast cancer in ‘high risk’ patients supplemented with nutritional antioxidants, essential fatty acids and coenzyme Q10. Mol Aspects Med. 1994;15 Suppl:s231-40.
14.)  Folkers K, Brown R, Judy WV, Morita M. Survival of cancer patients on therapy with coenzyme Q10. Biochem Biophys Res Commun. 1993 Apr 15;192(1):241-5.

Vitamin C – high dose or IV

1.) Yeom CH, Jung GC, Song KJ. Changes of terminal cancer patients’ health-related quality of life after high dose vitamin C administration. J Korean Med Sci. 2007 Feb;22(1):7-11.
2.) Shoichiro Ohtani, Arifumi Iwamaru, Wuguo Deng, Kentaro Ueda, Guanglin Wu, Gitanjali Jayachandran, Seiji Kondo, Edward N. Atkinson, John D. Minna, Jack A. Roth and Lin Ji. Tumor Suppressor 101F6 and Ascorbate Synergistically and Selectively Inhibit Non–Small Cell Lung Cancer Growth by Caspase-Independent Apoptosis and Autophagy. Cancer Research 67, 6293-6303, July 1, 2007.
3.) Sebastian J. Padayatty, Hugh D. Riordan, Stephen M. Hewitt, Arie Katz, L. John Hoffer and Mark Levine. Intravenously administered vitamin C as cancer therapy: three cases. CMAJ
2006;174(7):937-42.
4.) Riordan HD, Casciari JJ, González MJ, Riordan NH, Miranda-Massari JR, Taylor P, Jackson JA.A pilot clinical study of continuous intravenous ascorbate in terminal cancer patients. PR
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Grape Seed Extract (Resveratrol)

1.) Li T, Fan GX, Wang W, Li T, Yuan YK. Resveratrol induces apoptosis, influences IL-6 and exerts immunomodulatory effect on mouse lymphocytic leukemia both in vitro and in vivo. Int
Immunopharmacol. 2007 Sep;7(9):1221-31.
2.) Golkar L, Ding XZ, Ujiki MB, Salabat MR, Kelly DL, Scholtens D, Fought AJ, Bentrem DJ, Talamonti MS, Bell RH, Adrian TE. Resveratrol inhibits pancreatic cancer cell proliferation through transcriptional induction of macrophage inhibitory cytokine-1. J Surg Res. 2007 Apr;138(2):163-9.
3.) Gill C, Walsh SE, Morrissey C, Fitzpatrick JM, Watson RW.Resveratrol sensitizes androgen independent prostate cancer cells to death-receptor mediated apoptosis through multiple
mechanisms. Prostate. 2007 Nov 1;67(15):1641-53.
4.) Chen Y, Tseng SH. Pro- and anti-angiogenesis effects of resveratrol. In Vivo. 2007 Mar-Apr;21(2):365-70.
5.) Hudson TS, Hartle DK, Hursting SD, Nunez NP, Wang TT, Young HA, Arany P, Green JE. Inhibition of prostate cancer growth by muscadine grape skin extract and resveratrol through distinct mechanisms. Cancer Res. 2007 Sep 1;67(17):8396-405.
6.) Aziz MH, Nihal M, Fu VX, Jarrard DF, Ahmad N. Resveratrol-caused apoptosis of human prostate carcinoma LNCaP cells is mediated via modulation of phosphatidylinositol
3′-kinase/Akt pathway and Bcl-2 family proteins. Mol Cancer Ther. 2006 May;5(5):1335-41.
7.) Delmas D, Lancon, A, Colin, D, Jannin, B, Latruffe N. Resveratrol as a chemopreventative agent: a promising molecule for fighting cancer. Current Drug Targets. 2006 April; 7(4): 423-42.
8.) Garvin S, Ollinger, K, Dabrosin, C. Resveratrol induces apoptosis and inhibits angiogenesis in human breast cancer xenografts in vivo. Cancer Letters. 2006 Jan; 231(1): 113-22.
9.) Benitez DA, Pozo-Guisado E, Alvarez-Barrientos A, Fernandez-Salguero PM, Castellón EA. Mechanisms involved in resveratrol-induced apoptosis and cell cycle arrest in prostate
cancer-derived cell lines. J Androl. 2007 Mar-Apr;28(2):282-93. Epub 2006 Oct 18.
10.) Horvath Z, Saiko P, Illmer C, Madlener S, Hoechtl T, Bauer W, Erker T, Jaeger W, Fritzer-Szekeres M, Szekeres T. Resveratrol, an ingredient of wine, acts synergistically with Ara-C and tiazofurin in HL-60 human promyelocytic leukemia cells. Nucleosides Nucleotides Nucleic Acids. 2006;25(9-11):1019-24.
11.) Sexton E, Van Themsche C, LeBlanc K, Parent S, Lemoine P, Asselin E. Resveratrol interferes with AKT activity and triggers apoptosis in human uterine cancer cells. Mol Cancer. 2006 Oct 17;5:45.
12.) Jazirehi AR, Bonavida B. Resveratrol modifies the expression of apoptotic regulatory proteins and sensitizes non-Hodgkin’s lymphoma and multiple myeloma cell lines to paclitaxel-induced apoptosis. Mol Cancer Ther. 2004 Jan;3(1):71-84.
13.) Kim YA, Rhee SH, Park KY, Choi YH. Antiproliferative effect of resveratrol in human prostate carcinoma cells. J Med Food. 2003 Winter;6(4):273-80.
14.) Tyagi A, Agarwal R, Agarwal C. Grape seed extract inhibits EGF-induced and constitutively active mitogenic signaling but activates JNK in human prostate carcinoma DU145 cells: possible role in antiproliferation and apoptosis. Oncogene. 2003 Mar 6;22(9):1302-16.
15.) ng XZ, Adrian TE. Resveratrol inhibits proliferation and induces apoptosis in human pancreatic cancer cells. Pancreas. 2002 Nov;25(4):e71-6.
16.) Lin HY, Shih A, Davis FB, Tang HY, Martino LJ, Bennett JA, Davis PJ. Resveratrol induced serine phosphorylation of p53 causes apoptosis in a mutant p53 prostate cancer cell line. J Urol. 2002 Aug;168(2):748-55.
17.) Ahmad N, Adhami VM, Afaq F, Feyes DK, Mukhtar H. Resveratrol causes WAF-1/p21-mediated G(1)-phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma A431 cells. Clin Cancer Res. 2001 May;7(5):1466-73.

Turmeric (Curcumin)

1.) Ji C, Cao C, Lu S, Kivlin R, Amaral A, Kouttab N, Yang H, Chu W, Bi Z, Di W, Wan Y. Curcumin attenuates EGF-induced AQP3 up-regulation and cell migration in human ovarian cancer cells.Cancer Chemother Pharmacol. 2008 Jan 23 [Epub ahead of print].
2.) Steward WP, Gescher AJ. Curcumin in cancer management: Recent results of analogue design and clinical studies and desirable future research. Mol Nutr Food Res. 2008 Jan 9 [Epub ahead of print].
3.) Shankar S, Ganapathy S, Chen Q, Srivastava RK. Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis and angiogenesis. Mol Cancer. 2008 Jan 29;7(1):16 [Epub ahead of print]
4.) Moiseeva EP, Almeida GM, Jones GD, Manson MM. Extended treatment with physiologic concentrations of dietary phytochemicals results in altered gene expression, reduced growth, and apoptosis of cancer cells. Mol Cancer Ther. 2007 Nov;6(11):3071-9.
5.) Shankar S, Chen Q, Sarva K, Siddiqui I, Srivastava RK. Curcumin enhances the apoptosis-inducing potential of TRAIL in prostate cancer cells: molecular mechanisms of apoptosis, migration and angiogenesis. J Mol Signal. 2007 Oct 4;2:10.
6.) Shankar S, Srivastava RK. Bax and Bak genes are essential for maximum apoptotic response by curcumin, a polyphenolic compound and cancer chemopreventive agent derived from turmeric, Curcuma longa. Carcinogenesis. 2007 Jun;28(6):1277-86. Epub 2007 Feb 2.
7.) Shankar S, Srivastava RK. Involvement of Bcl-2 family members, phosphatidylinositol 3′-kinase/AKT and mitochondrial p53 in curcumin (diferulolylmethane)-induced apoptosis in prostate cancer. Int J Oncol. 2007 Apr;30(4):905-18.
8.) Somers-Edgar TJ, Scandlyn MJ, Stuart EC, Le Nedelec MJ, Valentine SP, Rosengren RJ. The combination of epigallocatechin gallate and curcumin suppresses ERalpha-breast cancer cell growth in vitro and in vivo. Int J Cancer. 2007 Dec 20 [Epub ahead of print].
9.) Chen A, Xu J, Johnson AC. Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1. Oncogene. 2006 Jan 12;25(2):278-87.
10.) Wahl H, Tan L, Griffith K, Choi M, Liu JR. Curcumin enhances Apo2L/TRAIL-induced apoptosis in chemoresistant ovarian cancer cells. Gynecol Oncol. 2007 Apr;105(1):104-12. Epub 2006 Dec 15.
11.) Chen J, Wanming D, Zhang D, Liu Q, Kang J.Water-soluble antioxidants improve the antioxidant and anticancer activity of low concentrations of curcumin in human leukemia cells. Pharmazie. 2005 Jan;60(1):57-61.
12.) Deeb DD, Jiang H, Gao X, Divine G, Dulchavsky SA, Gautam SC. Chemosensitization of hormone-refractory prostate cancer cells by curcumin to TRAIL-induced apoptosis. J Exp Ther Oncol. 2005;5(2):81-91.
13.)Dobrovolskaia MA, Kozlov SV.: Inflammation and cancer: when NF-kappaB amalgamates the perilous partnership. Curr Cancer Drug Targets. 2005 Aug;5(5):325-44.
14.) Deeb D, Jiang H, Gao X, Hafner MS, Wong H, Divine G, Chapman RA, Dulchavsky SA, Gautam SC. Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing gand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation. Mol Cancer Ther. 2004 Jul;3(7):803-12.
15.) Van Erk MJ, Teuling E, Staal YC, Huybers S, Van Bladeren PJ, Aarts JM, Van Ommen B. Time- and dose-dependent effects of curcumin on gene expression in human colon cancer cells. J Carcinog. 2004 May 12;3(1):8.
16.)Ernst P.: The role of inflammation in the pathogenesis of gastric cancer. Aliment Pharmacol Ther. 1999 Mar;13 Suppl 1:13-8
17.) Menon LG, Kuttan R, Kuttan G. Anti-metastatic activity of curcumin and catechin. Cancer Lett 1999;141:159–65.
18.) Khafif A, Schantz SP, Chou TC, Edelstein D, Sacks PG. uantitation of chemopreventive synergism between (-)-epigallocatechin-3-gallate and curcumin in normal, premalignant
and malignant human oral epithelial cells. Carcinogenesis. 1998
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Vitamin D

1.) Lappe J, Travers-Gustafson D, Davies K, Recker R, Heaney R. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. American Journal of Clinical Nutrition. Am J Clin Nutr. 2007 Jun;85(6):1586-91.
2.) Ma Y, et al. Study presented at the 2007 centennial meeting of the American Association for Cancer Research (AACR), April 14 to 18, 2007, Los Angeles.
3.)Holick MF.: Vitamin D: Its role in cancer prevention and treatment. Prog Biophys Mol Biol. 2006 Mar 10;
4.) Schwartz GG, Eads D, Rao A, Cramer SD, Willingham MC, Chen TC, Jamieson DP, Wang L, Burnstein KL, Holick MF, Koumenis C.:Pancreatic cancer cells express 25-hydroxyvitamin D-1
alpha-hydroxylase and their proliferation is inhibited by the prohormone 25-hydroxyvitamin D3.Carcinogenesis. 2004 Jun;25(6):1015-26. Epub 2004 Jan 23.
5.) Wietrzyk J, Pelczynska M, Madej J, Dzimira S, Kusnierczyk H, Kutner A, Szelejewski W, Opolski A.: Toxicity and antineoplastic effect of (24R)-1,24-dihydroxyvitamin D3 (PRI-2191).Steroids. 2004 Sep;69(10):629-35.
6.) Vegesna V, O’Kelly J, Said J, Uskokovic M, Binderup L, Koeffle HP.: Ability of potent vitamin D3 analogs to inhibit growth of prostate cancer cells in vivo. Anticancer Res. 2003
Jan-Feb;23(1A):283-9.
7.) Grant WB. An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation. Cancer. 2002 Mar 15;94(6):1867-75.
8.) Majewski S, Skopinska M, Marczak M, Szmurlo A, Bollag W, Jablonska S.: Vitamin D3 is a potent inhibitor of tumor cell-induced angiogenesis. J Investig Dermatol Symp Proc. 1996
Apr;1(1):97-101.
9.) James SY, Mackay AG, Colston KW. Effects of 1,25 dihydroxyvitamin D3 and its analogues on induction of apoptosis in breast cancer cells. J Steroid Biochem Mol Biol. 1996
Jul;58(4):395-401.
10.) Schwartz GG, Hill CC, Oeler TA, Becich MJ, Bahnson RR.1,25-Dihydroxy-16-ene-23-yne-vitamin D3 and prostate cancer cell proliferation in vivo. Urology. 1995 Sep;46(3):365-9.
11.) Majewski S, Szmurlo A, Marczak M, Jablonska S, Bollag W.: Inhibition of tumor cell-induced angiogenesis by retinoids, 1,25-dihydroxyvitamin D3 and their combination.Cancer Lett. 1993
Nov 30;75(1):35-9.

Bromelain (anasas comosus)

1.)Kalra N, Bhui K, Roy P, Srivastava S, George J, Prasad S, Shukla Y.Regulation of p53, nuclear factor kappaB and cyclooxygenase-2 expression by bromelain through targeting mitogen-activated protein kinase pathway in mouse skin.Toxicol Appl Pharmacol. 2008 Jan
1;226(1):30-7. Epub 2007 Aug 23.
2.) Báez R, Lopes MT, Salas CE, Hernández M. In vivo antitumoral activity of stem pineapple (Ananas comosus) bromelain. Planta Med. 2007 Oct;73(13):1377-83. Epub 2007 Sep 24.
3.) Beuth J, Braun JM. Modulation of murine tumor growth and colonization by bromelaine, an extract of the pineapple plant (Ananas comosum L.).In Vivo. 2005 Mar-Apr;19(2):483-5.
4.) Wallace JM. Nutritional and botanical modulation of the inflammatory cascade–eicosanoids, cyclooxygenases, and lipoxygenases–as an adjunct in cancer therapy. Integr Cancer Ther.
2002 Mar;1(1):7-37; discussion 37.
5.) Maurer HR.Bromelain: biochemistry, pharmacology and medical use. Cell Mol Life Sci. 2001 Aug;58(9):1234-45.
6.) Desser L, Holomanova D, Zavadova E, Pavelka K, Mohr T, Herbacek I. Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S10-5.
7.) Beuth J, Ost B, Pakdaman A, Rethfeldt E, Bock PR, Hanisch J, Schneider B. Impact of complementary oral enzyme application on the postoperative treatment results of breast cancer patients–results of an epidemiological multicentre retrolective cohort study. Cancer
Chemother Pharmacol. 2001 Jul;47 Suppl:S45-54.
8.) Tysnes BB, Maurer HR, Porwol T, Probst B, Bjerkvig R, Hoover F. Bromelain reversibly inhibits invasive properties of glioma cells.Neoplasia. 2001 Nov-Dec;3(6):469-79.
9.) Dale PS, Tamhankar CP, George D, Daftary GV. Co-medication with hydrolytic enzymes in radiation therapy of uterine cervix: evidence of the reduction of acute side effects. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S29-34.
10.) Hubarieva HO, Kindzel’s’kyĭ LP, Ponomar’ova OV, Udatova TV, Shpil’ova SI, Smolanka II, Korovin SI, Ivankin VS. Systemic enzymotherapy as a method of prophylaxis of postradiation
complications in oncological patients] Lik Sprava. 2000 Oct-Dec;(7-8):94-100.
11.) Eckert K, Grabowska E, Stange R, Schneider U, Eschmann K, Maurer HR. Effects of oral bromelain administration on the impaired immunocytotoxicity of mononuclear cells from mammary tumor patients. Oncol Rep. 1999 Nov-Dec;6(6):1191-9.
12.) Zavadova E, Desser L, Mohr T. Stimulation of reactive oxygen species production and cytotoxicity in human neutrophils in vitro and after oral administration of a polyenzyme preparation. Cancer Biother. 1995 Summer;10(2):147-52.
13.) Taussig SJ, Batkin S. Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharmacol. 1988 Feb-Mar;22(2):191-203.
14.) Batkin S, Taussig SJ, Szekerezes J. Antimetastatic effect of bromelain with or without its proteolytic and anticoagulant activity. J Cancer Res Clin Oncol. 1988;114(5):507-8.

Melatonin

1.) Lissoni P, Barni S, Mandalà, et al. Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal hormone melatonin in metastatic solid tumour patients with poor clinical status. Eur J Cancer 1999;35:1688–92.
2.) Lissoni P, Cazzanga M, Tancini G, et al. Reversal of clinical resistance to LHRH analogue in metastatic prostate cancer by the pineal hormone melatonin: efficacy of LHRH analogue plus melatonin in patients progressing on LHRH analogue alone. Eur Urol 1997;31:178–81.
3.) Lissoni P, Paolorossi F, Tancini G, et al. Is there a role for melatonin in the treatment of neoplastic cachexia? Eur J Cancer 1996;32A:1340–3.
4.) Lissoni P, Paolorossi F, Tancini G, et al. A phase II study of tamoxifen plus melatonin in metastatic solid tumour patients. Br J Cancer 1996;74:1466–8.
5.) Lissoni P, Brivio O, Brivio F, et al. Adjuvant therapy with the pineal hormone melatonin in patients with lymph node relapse due to malignant melanoma. J Pineal Res 1996;21:239–42.
6.) Lissoni P, Barmo S. Meregalli S, et al. Modulation of cancer endocrine therapy by melatonin: a phase II study of tamoxifen plus melatonin in metastatic breast cancer patients progressing under tamoxifen alone. Br J Cancer 1995;71:854–6.
7.) Reiter RJ, Melchiorri D, Sewerynek E, Poeggeler B, Barlow-Walden L, Chuang J, Ortiz GG, Acuna-Castroviejo D.: A review of the evidence supporting melatonin’s role as an antioxidant.J
Pineal Res. 1995 Jan;18(1):1-11.
8.) Neri B, Fiorelli C, Moroni F, et al. Modulation of human lymphoblastoid interferon activity by melatonin in metastatic renal cell carcinoma. Cancer 1994;73:315–9.
9.) Lissoni P, Barni S, Cazzaniga M, Ardizzoia A, Rovelli F, Brivio F, Tancini G.: Efficacy of the concomitant administration of the pineal hormone melatonin in cancer immunotherapy with low-dose IL-2 in patients with advanced solid tumors who had progressed on IL-2 alone. Oncology. 1994 Jul-Aug;51(4):344-7.
10.) Lissoni P, Barni S, Ardizzoia A, et al. A randomized study with the pineal hormone melatonin versus supportive care alone in patients with brain metastases due to solid neoplasms. Cancer 1994;73:699–701.
11.) Lissoni P, Barni S, Tancini G, et al. A randomised study with subcutaneous low-dose interleukin 2 alone vs interleukin 2 plus the pineal neurohormone melatonin in advanced solid neoplasms other than renal cancer and melanoma. Br J Cancer 1994;69:196–9.
12.) Aldeghi R, Lissoni P, Barni S, et al. Low-dose interlekin-2 subcutaneous immunotherapy in association with the pineal hormone melatonin as a first-line therapy in locally advanced or metastatic hepatocellular carcinoma. Eur J Cancer 1994;30A:167–70.
13.) Lissoni P, Brivio F, Ardizzoia A, et al. Subcutaneous therapy with low-dose interlekin-2 plus the neurohormone melatonin in metastatic gastric cancer patients with low performance status.
Tumori 1993;79:401–4.
14.) Lissoni P, Barni S, Ardizzoia A, et al. Randomized study with the pineal hormone melatonin versus supportive care alone in advanced nonsmall cell lung cancer resistant to a first-line
chemotherapy containing cisplatin. Oncology 1992;49:336–9.
15.) Lissoni P, Barni S, Crispino S, et al. Endocrine and immune effects of melatonin therapy in metastatic cancer patients. Eur J Cancer Clin Oncol 1989;25:789–95.

Calcium D-glucarate

1.) Singh J, Gupta KP. Induction of apoptosis by calcium D-glucarate in 7,12-dimethyl benz [a] anthracene-exposed mouse skin. J Environ Pathol Toxicol Oncol. 2007;26(1):63-73.
2.) Hanausek M, Walaszek Z, Slaga TJ. Detoxifying cancer causing agents to prevent cancer. Integr Cancer Ther. 2003 Jun;2(2):139-44.
3.) Calcium-D-glucarate. Altern Med Rev. 2002 Aug;7(4):336-9.[No authors listed].
4.) Walaszek Z, Szemraj J, Narog M, Adams AK, Kilgore J, Sherman U, Hanausek M. Metabolism, uptake, and excretion of a D-glucaric acid salt and its potential use in cancer prevention. Cancer Detect Prev. 1997;21(2):178-90.
5.) Heerdt AS, Young CW, Borgen PI. Calcium glucarate as a chemopreventive agent in breast cancer. Isr J Med Sci. 1995 Feb-Mar;31(2-3):101-5.

Di-indolymethanes (DIM, IC3)

1.) Moiseeva EP, Almeida GM, Jones GD, Manson MM.Extended treatment with physiologic concentrations of dietary phytochemicals results in altered gene expression, reduced growth, and apoptosis of cancer cells. Mol Cancer Ther. 2007 Nov;6(11):3071-9.
2.) Weng JR, Tsai CH, Kulp SK, Wang D, Lin CH, Yang HC, Ma Y, Sargeant A, Chiu CF, Tsai MH, Chen CS. A potent indole-3-carbinol derived antitumor agent with pleiotropic effects on multiple signaling pathways in prostate cancer cells. Cancer Res. 2007 Aug
15;67(16):7815-24.
3.) Pappa G, Strathmann J, Löwinger M, Bartsch H, Gerhäuser C. Quantitative combination effects between sulforaphane and 3,3′-diindolylmethane on proliferation of human colon cancer cells in vitro. Carcinogenesis. 2007 Jul;28(7):1471-7. Epub 2007 Feb 28.
4.) Pappa G, Lichtenberg M, Iori R, Barillari J, Bartsch H, Gerhäuser C. Comparison of growth inhibition profiles and mechanisms of apoptosis induction in human colon cancer cell lines
by isothiocyanates and indoles from Brassicaceae. Mutat Res. 2006 Jul 25;599(1-2):76-87. Epub 2006 Feb 24.
5.) Bhuiyan MM, Li Y, Banerjee S, Ahmed F, Wang Z, Ali S, Sarkar FH. Down-regulation of androgen receptor by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in both hormone-sensitive LNCaP and insensitive C4-2B prostate cancer cells. Cancer Res. 2006 Oct 15;66(20):10064-72.
6.) Aggarwal BB, Ichikawa H. Molecular targets and anticancer potential of indole-3-carbinol and its derivatives. Cell Cycle. 2005 Sep;4(9):1201-15. Epub 2005 Sep 6.
7.) Chinni SR, Li Y, Upadhyay S, Koppolu PK, Sarkar FH. Indole-3-carbinol (I3C) induced cell growth inhibition, G1 cell cycle arrest and apoptosis in prostate cancer cells. Oncogene. 2001
May 24;20(23):2927-36.
8.) Cover CM, Hsieh SJ, Cram EJ, et al. Indole-3-carbinol and tamoxifen cooperate to arrest the cell cycle of MCF-7 human breast cancer cells. Cancer Res 1999;59:1244–51.

Lycopene

1.) Parsons JK, Newman VA, Mohler JL, Pierce JP, Flatt S, Marshall J. Dietary modification in patients with prostate cancer on active surveillance: a randomized, multicentre feasibility study. BJU Int. 2008 Jan 24 [Epub ahead of print].
2.) Wang A, Zhang L.[Effect of lycopene on proliferation and cell cycle of hormone refractory prostate cancer PC-3 cell line]. Wei Sheng Yan Jiu. 2007 Sep;36(5):575-8.
3.) Gunasekera RS, Sewgobind K, Desai S, Dunn L, Black HS, McKeehan WL, Patil B. Lycopene and lutein inhibit proliferation in rat prostate carcinoma cells. Nutr Cancer. 2007;58(2):171-7.
4.) Vaishampayan U, Hussain M, Banerjee M, Seren S, Sarkar FH, Fontana J, Forman JD, Cher ML, Powell I, Pontes JE, Kucuk O. Lycopene and soy isoflavones in the treatment of prostate cancer. Nutr Cancer. 2007;59(1):1-7.
5.) Zhang J, Dhakal I, Stone A, Ning B, Greene G, Lang NP, Kadlubar FF. Plasma carotenoids and prostate cancer: a population-based case-control study in Arkansas. Nutr Cancer. 2007;59(1):46-53.
6.) Hwang ES, Bowen PE. Effects of lycopene and tomato paste extracts on DNA and lipid oxidation in LNCaP human prostate cancer cells. Biofactors. 2005;23(2):97-105.
7.) Hantz HL, Young LF, Martin KR. Physiologically attainable concentrations of lycopene induce mitochondrial apoptosis in LNCaP human prostate cancer cells. Exp Biol Med (Maywood). 2005 Mar;230(3):171-9.
8.) Giovannucci E, Rimm EB, Liu Y, Stampfer MJ, Willett WC. A prospective study of tomato products, lycopene, and prostate cancer risk. J Natl Cancer Inst. 2002 Mar 6;94(5):391-8.
9.) Levy J, Bosin E, Feldman B, et al. Lycopene is a more potent inhibitor of human cancer cell proliferation than either a-carotene or ß-carotene. Nutr Cancer 1995;24:257–66.
10.) Giovannucci E. Tomatoes, tomato-based products, lycopene, and cancer: review of the epidemiologic literature. J Natl Cancer Inst 1999;91:317–31.

Larch arabinogalactin

1.) Sathisha UV, Jayaram S, Harish Nayaka MA, Dharmesh SM. Inhibition of galectin-3 mediated cellular interactions by pectic polysaccharides from dietary sources. Glycoconj J. 2007 Nov;24(8):497-507. Epub 2007 May 25.
2.) Choi EM, Kim AJ, Kim YO, Hwang JK. Immunomodulating activity of arabinogalactan and fucoidan in vitro. J Med Food. 2005 Winter;8(4):446-53.
3.) Larch arabinogalactan. Altern Med Rev. 2000 Oct;5(5):463-6. [NO AUTHORS LISTED].
4.) Kelly GS. Larch arabinogalactan: clinical relevance of a novel immune-enhancing polysaccharide. Altern Med Rev. 1999 Apr;4(2):96-103.
5.) Hagmar B, Ryd W, Skomedal H.Arabinogalactan blockade of experimental metastases to liver by murine hepatoma. Invasion Metastasis. 1991;11(6):348-55.
6.) Beuth J, et al.. Inhibition of liver tumor cell colonization in two animal tumor models by lectin blocking with D-galactose or arabinogalactan. Clin Exp Metastasis 1988;6:115–20.
7.) Hirai O, Fujitsu T, Mori J, Kikuchi H, Koda S, Fujioka M, Morimoto Y. Antitumour activity of purified arabinogalactan-peptidoglycan complex of the cell wall skeleton of
Rhodococcus lentifragmentus. J Gen Microbiol. 1987 Feb;133(2):369-73.

Modified Citrus Pectin

1.) Sathisha UV, Jayaram S, Harish Nayaka MA, Dharmesh SM. Inhibition of galectin-3 mediated cellular interactions by pectic polysaccharides from dietary sources. Glycoconj J. 2007
Nov;24(8):497-507. Epub 2007 May 25.
2.) Jackson CL, Dreaden TM, Theobald LK, Tran NM, Beal TL, Eid M, Gao MY, Shirley RB, Stoffel MT, Kumar MV, Mohnen D. Pectin induces apoptosis in human prostate cancer cells: correlation of apoptotic function with pectin structure. Glycobiology. 2007 Aug;17(8):805-19. Epub 2007 May 19.
3.) Chen CH, Sheu MT, Chen TF, Wang YC, Hou WC, Liu DZ, Chung TC, Liang YC. Suppression of endotoxin-induced proinflammatory responses by citrus pectin through blocking LPS signaling pathways. Biochem Pharmacol. 2006 Oct 16;72(8):1001-9. Epub 2006 Aug 22.
4.) Glinskii OV, Huxley VH, Glinsky GV, Pienta KJ, Raz A, Glinsky VV.Mechanical entrapment is insufficient and intercellular adhesion is essential for metastatic cell arrest in distant organs.
Neoplasia. 2005 May;7(5):522-7.
5.) Guess BW, Scholz MC, Strum SB, Lam RY, Johnson HJ, Jennrich RI. Modified citrus pectin (MCP) increases the prostate-specific antigen doubling time in men with prostate cancer: a phase II pilot study. Prostate Cancer Prostatic Dis. 2003;6(4):301-4.
6.) Pratima Nangia-Makker, Victor Hogan, Yuichiro Honjo, Sara Baccarini, Larry Tait, Robert Bresalier, Avraham Raz. Inhibition of Human Cancer Cell Growth and Metastasis in Nude Mice by Oral Intake of Modified Citrus Pectin. J Natl Cancer Inst, Vol. 94, No. 24, December 18, 2002
7.) Nangia-Makker P, Hogan V, Honjo Y, Baccarini S, Tait L, Bresalier R, Raz A. Inhibition of human cancer cell growth and metastasis in nude mice by oral intake of modified citrus pectin. J Natl Cancer Inst. 2002 Dec 18;94(24):1854-62.
8.) Pienta KJ, Naik H, Akhtar A, Yamazaki K, Replogle TS, Lehr J, et al. Inhibition of spontaneous metastasis in a rat prostate cancer model by oral administration of modified citrus pectin. J Natl Cancer Inst 1995;87:348–53.
9.) Hsieh TC, Wu JM. Changes in cell growth, cyclin/kinase, endogenous phosphoproteins and nm23 gene expression in human prostatic JCA-1 cells treated with modified citrus pectin. Biochem Mol Biol Int. 1995 Nov;37(5):833-41.
10.) Platt D, Raz A. Modulation of the lung colonization of B16-F1 melanoma cells by citrus pectin. J Natl Cancer Inst. 1992 Mar 18;84(6):438-42.

 

Natural Strategies To Help Avoid Cancer

What is Cancer?
The word “cancer” is a general term used to describe body cells that grow uncontrollably and often invade other body tissue. Benign tumors are also body cells that multiply, but they do not grow uncontrollably and invade other parts of the body. Cancer can begin in virtually any part of the body. The most common locations for cancer are the lungs, colon, breast, and prostate.

How does Cancer start?
Scientists believe that cancer starts as a single cell with altered chromosomes. Chromosomes are the “brain” inside each cell in the body. Chromosomes tell the cell how to behave.

In cancer cells, abnormal chromosomes give rise to abnormal cell behavior. Such abnormal behavior includes rapid multiplication of cells. Unlike normal cells, cancer cells do not stop growing when they reach a particular number. Instead, they continue to multiply, pushing on vital organs, robbing the “host” of nutrients, and spreading to other parts of the body by way of the lymphatic or blood-vascular system. (A process called “metastasis”).

What Causes Cancer?
Altered chromosomes inside the cell are ultimately thought to be responsible for abnormal cell behavior. But what causes chromosomes to become altered?

A number of factors are known to alter chromosomes. Some of these alterations may be pre-programmed into a cell; what we would call “genetic.” A person may be born with such abnormal chromosomes.

Other factors that are known to damage chromosomes and initiate cancer are known as carcinogens. These appear to be a far more common cause of cancer. Carcinogenic substances include ionizing radiation, smoke, and a wide variety of chemicals. Chronic irritation of any body tissue can also cause a cell to become cancerous.

Cancer and the Immune System
Scientists have demonstrated that a normal body produces approximately 300 or more cancerous cells per day. So why doesn’t everyone develop cancer? The answer lies in the immune system, a portion of the body that is designed to protect us from foreign “invasion.” In a body with a healthy immune system, cancer cells are recognized and destroyed. This process occurs inside everyone, all the time, every day. When the immune system is “compromised’ for any reason – for example, from nutritional deficiencies, cigarette smoking, or excessive physical or emotional stress – it may fail to identify cancerous cells. Once a cancerous cell begins to multiply, it becomes more difficult for the immune system to contain it. (Think of a wild fire. Very early, it is easy to put out. Let it “grow” for a while, and it becomes more dangerous).

Diagnosis of Cancer
There is no early blood or other tests that will tell us when an aberrant cell has escaped immune system recognition. In fact, our current diagnosis of cancer usually relies on a “mass,” or noticeable tumor, being present. Mammography, a low dose X-ray picture taken of the female breast, is an example of an early detection method. Though often touted as “prevention,” it is not. Diagnostic test are a means of early detection of cancer. They are NOT preventive measures.

The “War on Cancer”
President Nixon signed a bill on December 23, 1971, declaring an all-out “war” on cancer. This bill opened a floodgate of federal funding to research a cure for cancer. Since the signing of this bill, tens of billions of dollars of federal money, and additional private sector money, have been spent on this “war on cancer.”

Don’t let anyone fool you: it’s a “war” we’re losing. Since the signing of this bill, the death rate from cancer has risen. Some people will tell you these statistics are inaccurate because people are living longer, but this, too, is a falsehood. These numbers are age adjusted.

Common cancers, such as lung cancer, are increasingly common. Prostate and brain cancers and non-Hodgkin’s lymphoma are beginning to rise in the general population. So are a number of other types of cancer.

Conventional Treatment of Cancer
Like the stories that suggest that we are winning the “war on cancer,” conventional treatment improvements are a myth. There has been little significant advancement in the treatment of cancer in the past twenty years.

What has improved is our ability to detect cancer earlier, when it is still curable by surgery alone. Radiation and chemotherapy can provide a margin of additional “time” in a few types of cancer, but often at the expense of quality of life.

Surgery still remains one of the best conventional treatments for cancer, and then, it is most effective when the cancer is detected early. Surgery is also more effective when the immune system is otherwise strong and healthy.

Don’t misunderstand me. There are some advances in survival times with the use of certain drugs. For example, the anti-estrogen drug Tamoxifen improves survival times in post menopausal women with hormone-responsive breast cancer. Of course, if these women were “stage I” or “stage II’ when their cancer was removed, the chance of recurrence of cancer is very low anyway. Again, this is an indication that early detection and surgical removal remains one of our most effective conventional treatments. Certain nutritional supplements should sometimes be avoided during chemotherapy because they can reduce the effectiveness of the drugs, but most supplements actually minimize negative side-effects of chemotherapy and radiation. And there are some types of cancers that, although present in a body, should probably be left alone because they are unlikely to spread.

All of these questions need to be answered with the assistance of an holistic physician who can help you determine the best course of action to take and will work with you to sort out the legitimate treatments from the “hype.” There is no room for guesswork and inexperience once a diagnosis of cancer has been made. Please consider obtaining a consultation with Dr. Myatt.

Prevention is the Best “Cure”
Modern medical science may not know much more about treating cancer than it did twenty years ago, but we do know a lot more about prevention. At this point in medical history, it’s fair to say that prevention of cancer is a surer and safer bet than cure.

DIET AND LIFESTYLE RECOMMENDATIONS

• Maintain a normal weight. Excess body fat is associated with a number of cancers, including postmenopausal breast cancer and prostate cancer.
• Eat a diet rich in antioxidant nutrient foods (fruits and vegetables). Include “Super Foods” lavishly. Use soy and soy products if tolerated. Buy organic produce whenever possible.
• Do not smoke. Limit alcohol consumption.
• Drink pure water, not tap water. Chlorine byproducts are can cause urinary tract and other cancers. Other contaminants in water have unknown effects but many are believed to relate to cancer.
• Exercise regularly. Many types of cancers (ovarian, breast, prostate, colon) occur far less often (up to 50% less) in people who engage in regular physical activity. [Ref.: N. Eng. J. Med. 338:94,1998]
• Practice “Emotional hygiene.” Emotional distress (“stress”) suppresses the immune system and may make a person more susceptible to cancer and other diseases. Conversely, optimism is associated with improved immunity in a number of studies. Watch The Body/Mind Connection video to learn exactly how this occurs.

 

PRIMARY SUPPORT:

 

• Maxi Multi: 3 caps, 3 times per day with meals. Optimal (not minimal) doses of all nutrients are important in preventing cancer, since a single micronutrient deficiency can cause immune system weakness. Antioxidants (A, C, carotene and selenium), and vitamin D are especially important.
• Maxi Greens: 3 caps, 3 times daily with meals for complete phytonutrient coverage.
• Omega 3 fatty acids:
  Flax seed meal, 2 teaspoons per day with food
  OR
  Flax seed capsules: 2-4 caps, 3 times per day (target dose range: 6-12 caps per day)
  OR
  Flax seed oil: 1-2 tablespoons per day
  OR
  Max EPA (Omega-3 rich fish oil): 1-2 caps, 3 times per day with meals (target dose: 3-6 caps per day).

 

ADDITIONAL SUPPORT

 

• Diindolymethane (DIM): 2 caps, 2 times per day.
• Turmeric: 1 caps, 2-3 times per day with meals.
• Melatonin: 3-5mg at bedtime

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References

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Super Foods

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Smoking, Alcohol and Cancer Risk

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Drinking Water and Cancer Risk

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Exercise and Cancer

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Emotional Hygiene and The immune System

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Multiple Vitamins and Cancer

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2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
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Antioxidants (General) and Cancer

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Vitamin A and Carotenes

1.) Yuan JM, Ross RK, Gao YT, Qu YH, Chu XD, Yu MC. Prediagnostic levels of serum micronutrients in relation to risk of gastric cancer in Shanghai, China. Cancer Epidemiol Biomarkers Prev. 2004 Nov;13(11 Pt 1):1772-80.
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8.) Pastorino U, Infante M, Maioli M, et al. Adjuvant treatment of stage I lung cancer with high-dose vitamin A. J Clin Oncol 1993;11:1216–22.

Vitamin C

1.) Wybieralska E, Koza M, Sroka J, Czyz J, Madeja Z. Ascorbic acid inhibits the migration of walker 256 carcinosarcoma cells. Cell Mol Biol Lett. 2008;13(1):103-11. Epub 2007 Oct 29.
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4.) Bussey HJR, DeCosse JJ, Deschner EE, et al. A randomized trial of ascorbic acid in polyposis coli. Cancer 1982;50:1434–9.
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Selenium

1.) Li H, Stampfer MJ, Giovannucci EL, Morris JS, Willett WC, Gaziano JM, Ma J.A prospective study of plasma selenium levels and prostate cancer risk. J Natl Cancer Inst. 2004 May
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2.) Yu M-W, Horng I-S, Hsu K-H, et al. Plasma selenium levels and risk of hepatocellular carcinoma among men with chronic hepatitis virus infection. Am J Epidemiol 1999;150:367–74.
3.) Knekt P, Marniemi J, Teppo L, et al. Is low selenium status a risk factor for lung cancer? 1998 Nov 15;148(10):975-82.
4.) Scieszka M, Danch A, Machalski M, Drozdz M. Plasma selenium concentration in patients with stomach and colon cancer in the Upper Silesia. Neoplasma 1997;44:395–7.
5.) Toma S, Micheletti A, Giacchero A, et al. Selenium therapy in patients with precancerous and malignant oral cavity lesions: preliminary results.Cancer Detection Prev 1991;15:491–3.
6.) Knekt P, Aromaa A, Maatela J, et al. Serum selenium and subsequent risk of cancer among Finnish men and women. J Natl Cancer Inst 1990;82:864–8.
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Vitamin D

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Omega 3 Essential Fatty Acids

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7.) Espada CE, Berra MA, Martinez MJ, Eynard AR, Pasqualini ME. Effect of Chia oil (Salvia Hispanica) rich in omega-3 fatty acids on the eicosanoid release, apoptosis and T-lymphocyte tumor infiltration in a murine mammary gland adenocarcinoma. Prostaglandins Leukot Essent Fatty Acids. 2007 Jul;77(1):21-8. Epub 2007 Jul 6.
8.) Saarinen NM, Power K, Chen J, Thompson LU. Flaxseed attenuates the tumor growth stimulating effect of soy protein in ovariectomized athymic mice with MCF-7 human breast cancer xenografts. Int J Cancer. 2006 Aug 15;119(4):925-31.
9.) Shirota T, Haji S, Yamasaki M, Iwasaki T, Hidaka T, Takeyama Y, Shiozaki H, Ohyanagi H. Apoptosis in human pancreatic cancer cells induced by eicosapentaenoic acid. Nutrition. 2005 Oct;21(10):1010-7.
10.) Schley PD, Jijon HB, Robinson LE, Field CJ. Mechanisms of omega-3 fatty acid-induced growth inhibition in MDA-MB-231 human breast cancer cells. Breast Cancer Res Treat. 2005 July;92(2):187-95.
11.) de Deckere EA. Possible beneficial effect of fish and fish n-3 polyunsaturated fatty acids in breast and colorectal cancer. Eur J Cancer Prev. 1999 Jul;8(3):213-21.
12.) Chang WL, Chapkin RS, Lupton JR. Fish oil blocks azoxymethane-induced rat colon tumorigenesis by increasing cell differentiation and apoptosis rather than decreasing cell proliferation. J Nutr. 1998 Mar;128(3):491-7.
13.) Bagga D, Capone S, Wang HJ, Heber D, Lill M, Chap L, Glaspy JA. Dietary modulation of omega-3/omega-6 polyunsaturated fatty acid ratios in patients with breast cancer. J Natl Cancer Inst. 1997 Aug 6;89(15):1123-31.

Di-indolymethanes (DIM, IC3)

1.) Moiseeva EP, Almeida GM, Jones GD, Manson MM.Extended treatment with physiologic concentrations of dietary phytochemicals results in altered gene expression, reduced growth, and apoptosis of cancer cells. Mol Cancer Ther. 2007 Nov;6(11):3071-9.
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5.) Bhuiyan MM, Li Y, Banerjee S, Ahmed F, Wang Z, Ali S, Sarkar FH. Down-regulation of androgen receptor by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in both hormone-sensitive LNCaP and insensitive C4-2B prostate cancer cells. Cancer Res. 2006 Oct 15;66(20):10064-72.
6.) Aggarwal BB, Ichikawa H. Molecular targets and anticancer potential of indole-3-carbinol and its derivatives. Cell Cycle. 2005 Sep;4(9):1201-15. Epub 2005 Sep 6.
7.) Chinni SR, Li Y, Upadhyay S, Koppolu PK, Sarkar FH. Indole-3-carbinol (I3C) induced cell growth inhibition, G1 cell cycle arrest and apoptosis in prostate cancer cells. Oncogene. 2001 May 24;20(23):2927-36.
8.) Cover CM, Hsieh SJ, Cram EJ, et al. Indole-3-carbinol and tamoxifen cooperate to arrest the cell cycle of MCF-7 human breast cancer cells. Cancer Res 1999;59:1244–51.

Turmeric (Curcumin)

1.) Ji C, Cao C, Lu S, Kivlin R, Amaral A, Kouttab N, Yang H, Chu W, Bi Z, Di W, Wan Y. Curcumin attenuates EGF-induced AQP3 up-regulation and cell migration in human ovarian cancer cells.Cancer Chemother Pharmacol. 2008 Jan 23 [Epub ahead of print].
2.) Steward WP, Gescher AJ. Curcumin in cancer management: Recent results of analogue design and clinical studies and desirable future research. Mol Nutr Food Res. 2008 Jan 9 [Epub ahead of print].
3.) Shankar S, Ganapathy S, Chen Q, Srivastava RK. Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis and angiogenesis. Mol Cancer. 2008 Jan 29;7(1):16 [Epub ahead of print]
4.) Moiseeva EP, Almeida GM, Jones GD, Manson MM. Extended treatment with physiologic concentrations of dietary phytochemicals results in altered gene expression, reduced growth, and apoptosis of cancer cells. Mol Cancer Ther. 2007 Nov;6(11):3071-9.
5.) Shankar S, Chen Q, Sarva K, Siddiqui I, Srivastava RK. Curcumin enhances the apoptosis-inducing potential of TRAIL in prostate cancer cells: molecular mechanisms of apoptosis, migration and angiogenesis. J Mol Signal. 2007 Oct 4;2:10.
6.) Shankar S, Srivastava RK. Bax and Bak genes are essential for maximum apoptotic response by curcumin, a polyphenolic compound and cancer chemopreventive agent derived from turmeric, Curcuma longa. Carcinogenesis. 2007 Jun;28(6):1277-86. Epub 2007 Feb 2.
7.) Shankar S, Srivastava RK. Involvement of Bcl-2 family members, phosphatidylinositol 3′-kinase/AKT and mitochondrial p53 in curcumin (diferulolylmethane)-induced apoptosis in prostate cancer. Int J Oncol. 2007 Apr;30(4):905-18.
8.) Somers-Edgar TJ, Scandlyn MJ, Stuart EC, Le Nedelec MJ, Valentine SP, Rosengren RJ. The combination of epigallocatechin gallate and curcumin suppresses ERalpha-breast cancer cell growth in vitro and in vivo. Int J Cancer. 2007 Dec 20 [Epub ahead of print].
9.) Chen A, Xu J, Johnson AC. Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1. Oncogene. 2006 Jan 12;25(2):278-87.
10.) Wahl H, Tan L, Griffith K, Choi M, Liu JR. Curcumin enhances Apo2L/TRAIL-induced apoptosis in chemoresistant ovarian cancer cells. Gynecol Oncol. 2007 Apr;105(1):104-12. Epub 2006 Dec 15.
11.) Chen J, Wanming D, Zhang D, Liu Q, Kang J.Water-soluble antioxidants improve the antioxidant and anticancer activity of low concentrations of curcumin in human leukemia cells. Pharmazie. 2005 Jan;60(1):57-61.
12.) Deeb DD, Jiang H, Gao X, Divine G, Dulchavsky SA, Gautam SC. Chemosensitization of hormone-refractory prostate cancer cells by curcumin to TRAIL-induced apoptosis. J Exp Ther Oncol. 2005;5(2):81-91.
13.)Dobrovolskaia MA, Kozlov SV.: Inflammation and cancer: when NF-kappaB amalgamates the perilous partnership. Curr Cancer Drug Targets. 2005 Aug;5(5):325-44.
14.) Deeb D, Jiang H, Gao X, Hafner MS, Wong H, Divine G, Chapman RA, Dulchavsky SA, Gautam SC. Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing gand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation. Mol Cancer Ther. 2004 Jul;3(7):803-12.
15.) Van Erk MJ, Teuling E, Staal YC, Huybers S, Van Bladeren PJ, Aarts JM, Van Ommen B. Time- and dose-dependent effects of curcumin on gene expression in human colon cancer cells. J Carcinog. 2004 May 12;3(1):8.
16.)Ernst P.: The role of inflammation in the pathogenesis of gastric cancer. Aliment Pharmacol Ther. 1999 Mar;13 Suppl 1:13-8
17.) Menon LG, Kuttan R, Kuttan G. Anti-metastatic activity of curcumin and catechin. Cancer Lett 1999;141:159–65.
18.) Khafif A, Schantz SP, Chou TC, Edelstein D, Sacks PG. uantitation of chemopreventive synergism between (-)-epigallocatechin-3-gallate and curcumin in normal, premalignant and malignant human oral epithelial cells. Carcinogenesis. 1998

Melatonin

1.) Lissoni P, Barni S, Mandalà, et al. Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal hormone melatonin in metastatic solid tumour patients with poor clinical status. Eur J Cancer 1999;35:1688–92.
2.) Lissoni P, Cazzanga M, Tancini G, et al. Reversal of clinical resistance to LHRH analogue in metastatic prostate cancer by the pineal hormone melatonin: efficacy of LHRH analogue plus melatonin in patients progressing on LHRH analogue alone. Eur Urol 1997;31:178–81.
3.) Lissoni P, Paolorossi F, Tancini G, et al. Is there a role for melatonin in the treatment of neoplastic cachexia? Eur J Cancer 1996;32A:1340–3.
4.) Lissoni P, Paolorossi F, Tancini G, et al. A phase II study of tamoxifen plus melatonin in metastatic solid tumour patients. Br J Cancer 1996;74:1466–8.
5.) Lissoni P, Brivio O, Brivio F, et al. Adjuvant therapy with the pineal hormone melatonin in patients with lymph node relapse due to malignant melanoma. J Pineal Res 1996;21:239–42.
6.) Lissoni P, Barmo S. Meregalli S, et al. Modulation of cancer endocrine therapy by melatonin: a phase II study of tamoxifen plus melatonin in metastatic breast cancer patients progressing under tamoxifen alone. Br J Cancer 1995;71:854–6.
7.) Reiter RJ, Melchiorri D, Sewerynek E, Poeggeler B, Barlow-Walden L, Chuang J, Ortiz GG, Acuna-Castroviejo D.: A review of the evidence supporting melatonin’s role as an antioxidant.J Pineal Res. 1995 Jan;18(1):1-11.
8.) Neri B, Fiorelli C, Moroni F, et al. Modulation of human lymphoblastoid interferon activity by melatonin in metastatic renal cell carcinoma. Cancer 1994;73:315–9.
9.) Lissoni P, Barni S, Cazzaniga M, Ardizzoia A, Rovelli F, Brivio F, Tancini G.: Efficacy of the concomitant administration of the pineal hormone melatonin in cancer immunotherapy with low-dose IL-2 in patients with advanced solid tumors who had progressed on IL-2 alone. Oncology. 1994 Jul-Aug;51(4):344-7.
10.) Lissoni P, Barni S, Ardizzoia A, et al. A randomized study with the pineal hormone melatonin versus supportive care alone in patients with brain metastases due to solid neoplasms. Cancer 1994;73:699–701.
11.) Lissoni P, Barni S, Tancini G, et al. A randomised study with subcutaneous low-dose interleukin 2 alone vs interleukin 2 plus the pineal neurohormone melatonin in advanced solid neoplasms other than renal cancer and melanoma. Br J Cancer 1994;69:196–9.
12.) Aldeghi R, Lissoni P, Barni S, et al. Low-dose interlekin-2 subcutaneous immunotherapy in association with the pineal hormone melatonin as a first-line therapy in locally advanced or metastatic hepatocellular carcinoma. Eur J Cancer 1994;30A:167–70.
13.) Lissoni P, Brivio F, Ardizzoia A, et al. Subcutaneous therapy with low-dose interlekin-2 plus the neurohormone melatonin in metastatic gastric cancer patients with low performance status. Tumori 1993;79:401–4.
14.) Lissoni P, Barni S, Ardizzoia A, et al. Randomized study with the pineal hormone melatonin versus supportive care alone in advanced nonsmall cell lung cancer resistant to a first-line chemotherapy containing cisplatin. Oncology 1992;49:336–9.
15.) Lissoni P, Barni S, Crispino S, et al. Endocrine and immune effects of melatonin therapy in metastatic cancer patients. Eur J Cancer Clin Oncol 1989;25:789–95.

Dana Myatt, N.M.D. and Mark Ziemann, R.N.

Overview

Some types of cancer are consistently responsive to conventional medical treatment, especially those amenable to surgical intervention when diagnosed early. Cytotoxic therapy is helpful in selected instances. For most cancers, especially those advanced beyond Stage I or II, conventional treatments that evoke durable remissions are elusive and inconsistent. In many instances, cytotoxic and radiation therapies end a patient’s life sooner than the natural course of the disease would be expected to.

Alternative cancer therapies, while typically gentler and less inherently dangerous, have also proven inconsistent for evoking durable remissions. However, instances can be found where durable remissions and event apparent cure have been obtained by unconventional and alternative treatments used as stand-alone therapy. When used in conjunction with conventional treatments, alternative therapies can sometimes potentiate the positive effects of conventional therapy, mitigate the negative effects, or both.

The questions we will examine in this presentation include:

I.) Which alternative treatments are most effective as the sole treatment for malignancy and when should they be used?

II.) Which alternative treatments are most effective as adjuncts to conventional therapy?

III.) Which alternative treatments may be contraindicated for adjunct cancer therapy?

A careful review of the medical literature reveals that there are in fact specific modes of action to explain when and why alternative treatments are effective and when such treatments fail.

Cancer Cell Characteristics: Understanding the Enemy

Developing a cohesive and effective treatment strategy requires an understanding of the behavior and biology of cancer cells. Although various cancer types display unique behaviors, there are a number of characteristics common to all solid tissue malignancies:

1. Altered interactions with neighboring cells. Unlike normal cells whose division stops when neighboring cells are encountered, cancer cells continue to multiply with uncontrolled growth. This trait is known as lack of contact inhibition.

Normal cells require a solid substrate (basement membrane) upon which to grow. This is known as anchorage-dependent growth. Cancer cells are anchorage-independent, growing in circumstances where they are deprived of substrate.

2. Altered cellular metabolism. Cancer cells demonstrate a greatly increased rate of glucose transport. Anaerobic glycolysis is the predominant energy pathway of cancer cells, even in the presence of adequate oxygen. This may partly explain the large amount of metabolic acids produced by cancer cells.

Tumor cells have reduced growth requirements and will proliferate in culture media (less than 1% serum) that halt cell growth and division of normal cells.

3. Vascularization. Tumor cells secrete angiogenic growth factors which cause non-neoplastic blood vessels to grow from surrounding normal tissue. Research indicates that associated fibrin deposits many be necessary for angiogenesis. (1,2)

4. Invasion and metastasis. Multiple characteristics allow for local invasion and distant metastasis.

Cancer cells often secrete enzymes including collagenase, heparinase and stromolysin which are capable of degrading basement membrane and allowing invasion of tumor into adjacent tissues and general circulation.

Inflammation is caused by cellular substances, high acid cellular waste, and tumor pressure on adjacent normal tissue which produces histamine, leukotrienes and prostaglandins of the 2 series, increasing capillary permeability.

Anchorage independence (discussed above) allows cancer cells to travel through the blood stream without substrate. Normal cells do not have this ability. Once a clump of cancerous sells has made its way into general circulation, aggregates of platelets and/or fibrin encasement may serve as protection from the immune system.

Cancer cells have affinity for metastasis to certain and predictable locations not related to obvious blood flow patterns. Unidentified tissue chemotactic factors or lectin binding sites may account for this attraction. (3)

5. Escape from immune surveillance. Carcinogenic burden may simply overwhelm available immune surveillance, especially in the immunocompromised host.

Many cancer patients have apparently intact immune systems, however, and it is felt that cancer cells may secrete substances which circumvent the host’s immune response. Such immune-eluding substances include prostaglandins and other inflammatory substances. Fibrin and platelet aggregation may also serve to assist in protection from host immune response.

Tumor cells also appear to escape host immunity by down-regulation of Human Leukocytic Antigen (HLA) expression. HLA assists lymphocyte recognition of target cells.

Causes of Cancer

Understanding the causes of a particular cancer gives valuable clues to vulnerabilities and points of attack. Immune system dysfunction has long been considered a primary cause and point of treatment in alternative cancer treatment. However, there is significant evidence to suggest that immune dysfunction is only one of a number of causative factors and certainly NOT the most important one.

It appears that very few cancers have a single cause or “initiator.” Instead, most cancers may begin as a series of combination of events that lead to mutation. Tumor initiation begins when DNA in a cell or population of cells is damaged by exposure to exogenous or endogenous carcinogens. This alone is not sufficient to give rise to cancer. Damage at this point can be repaired. If DNA damage is not repaired or damaged cells eliminated, and if the microenvironment of the damaged calls are suitable to contribute to cell growth, then the process continues to the “promotion” phase. (48,49,50,51,52)

Known initiators of cancer include:

1. Genetic factors. A number of genetic factors may play a role in susceptibility to cancer, although study of this aspect of malignancy is a newly emerging field. (47) Such genetic factors include APC/MCC (45,46), RAS, DCC, p53 mutations and/or allelic losses, hyperexpression of c-MYC and RB genes. (10)

Mutation of the p53 tumor suppressor gene is the most frequently observed genetic lesion in human cancer; more than 50% of all human tumors examined to date have identifiable p53 gene point mutations or deletions. (4,5,6,7,14) While some p53 gene mutation is heritable, the majority of tumor suppressor gene mutation appears inducible, primarily by environmental factors. (8,9,11,12,13,15,16,17)

Although genetics undoubtedly play a role in susceptibility to cancer, it is estimated that less than 25% of all cancers are genetically related. (58)

2. 2.) Chronic viral infections. Chronic infections of Epstein-Barr(EBV) (18,19,20,21,32) ,Human Papilloma (HPV) (22,23,24,25), Hepatitis C (HCV) (26), Hepatitis B (HBV) (27), Cytomegalovirus (CMV) (28,29,30), human polyomaviruses JC(JCV) and BK (BKV) (31), and others predispose to cancer development.

3. 3.) Chronic inflammation.(32,33,34,35,36,37,38,39,40,41,42,43,44,47)

4. 4.) Toxins, both endogenous and exogenous, can initiate cancer by causing ROS which in turn damage DNA. A number of exogenous and endogenous chemicals are considered carcinogenic, although the rate and degree of internal detoxification, especially phase II liver enzymes, are an important part of the initiation process. Few substances are carcinogenic per se without contribution from faulty or under-functioning internal detoxification systems. (53,54,55,56,57,58,59)

5. 5.) Ionizing radiation. X-rays and other sources of ionizing radiation are known to cause DNA mutations consistent with cancer initiation. (60)

Cancer Promoters

DNA damage alone is usually insufficient to initiate tumor development. If the DNA damage is repaired or the damaged cell is eliminated, the multi-step process of cancer development will be thwarted. If, however, mutagenic damage is not repaired and/or the damaged cell is not eliminated, and if the cellular environment is conducive to cell growth, then damaged cells can multiply. This stage is known as “progression” and it is a necessary step for the development of malignancy. Factors which promote malignant cell growth include:

1.) Nutritional deficiencies. Certain vitamins, minerals, trace minerals and phytonutrients act in a number of ways to thwart malignant cell promotion. The mechanisms of actions are many and varied but include ROS inactivation, upregulation of detoxification pathways, esp. phase II liver enzyme pathways, direct decrease or neutralization of carcinogenic compounds, and immune system enhancement. Deficiencies of any one of the nutrients involved in these protective processes can leave the organism vulnerable to the promotion phase of cancer development.(61,62,63,64,65,66,67,68,69,70,71)

2.) Extracellular milieu. Blood glucose, insulin, cortisol, and arachadonic-derived prostatglandins (especially PGE2) act as promoters. In hormone-responsive cancers, estrogens, testosterone, prolactin and sex hormone metabolites and mimickers can also promote cell growth. The metabolic state of the organism therefore plays a major role in the promotion of cancer. (72,73,74,75,76,77)

3.) Inflammation. In addition to being an initiator of cancer, inflammation also acts to promote cancer in several ways, primarily by altering the cell-to-cell communication and delaying local detoxification. (32,33,34,35,37,38,39,40)

Treatment Strategies

Treatment strategies involve interfering with cancer progression at any phase of development, but initiation and promotion stages present the greatest opportunity for intervention.

To prevent the DNA damage which occurs during initiation, steps can be taken to mitigate sources of mutation, as follows:

I.) Genetic factors. While this aspect of initiation might seem the hardest to compensate for, it must be remembered that genetic mutation represents only weakness, not a forgone conclusion that cancer will develop. Minimizing other predispositions to initiation, such as nutrient deficiencies and carcinogenic exposure, can be sufficient to overcome heritable weaknesses. Further, dietary fasting, calorie restriction (CR) or a ketogenic diet (KD) have been shown to suppress the p53 oncogene, rendering this most common genetic factor less relevant. (78)

II.) Chronic viral infections. As with genetic factors, the presence of a chronic viral infection does not, by itself, mean an initiating certainly. Immune-enhancing strategies, anti-viral therapies and avoidance of other known initiators may be sufficient to prevent virally-caused mutagenesis.

III.) Chronic inflammation. Now known as a risk factor for heart disease, rheumatic disease and cancer, even subtle levels of inflammation, as measured by an hs-CRP blood test, can elevate risk of initiation. Fortunately, such inflammatory conditions respond well to nutritional, botanical and dietary modification. CR and KD have both been shown to reduce inflammation. Bromelain, curcumin and other anti-cancer drugs are, perhaps not coincidentally, also potent anti-inflammatory substances.

IV.) Toxins and radiation. Minimization of exposure and optimal dietary antioxidants can help offset the effects of environmental toxins, whether chemicals or ionizing radiation. Avoidance of exposure is also an obvious but often-overlooked preventive measure.

The Most Potent Anti-Cancer Strategy Known

“Attack by stratagem: hence, to fight and conquer in all your battles is not supreme excellence; supreme excellence consists in breaking the enemy’s resistance without fighting” —Sun Tzu, “The Art of War”

Nutritional and botanical factors can have profound positive effects in cancer treatment, either alone or as adjuncts to conventional treatment.

The single most potent anti-cancer strategy documented in the medical literature is to strike at the core of cancer’s metabolism: anaerobic glycolysis. Numerous animal and human studies have demonstrated that the glycolytic pathway of cancer cells can be confounded by the metabolic state of ketosis, often with profound apoptotic effects on cancer cells but without consequence to normal cells. In fact, the metabolic state of ketosis may curtail cancer growth by a number of different mechanisms:

I.) Greatly decreasing the glucose substrate required for cancer cell metabolism. Most tumors express abnormalities in the number and function of their mitochondria (80,81,88,89). Such abnormalities would prevent the bioenergetic utilization of ketone bodies, which require functional mitochondria for their oxidation.

II.) Decreasing insulin, a secondary growth factor for cancer cells.

III.) Decreasing inflammation (metabolic ketosis has anti-inflammatory effects). (85,86,87)

IV.) Decreasing ROS production. (82,83,84)

As one author pointed out, why would we believe that cells damaged by mutation are more resilient than normal cells? The answer is: they are not. Malignant cells are largely incapable of the metabolic flexibility displayed by normal cells, and therein lies their weakness and the potential for a gentle but highly effective point of attack.

Ketosis can be achieved by a high fat, moderate protein, low carbohydrate diet or by a calorie-restricted (CR) diet. Both methods of achieving ketosis have proven to decrease the production of ROS. Calorie restriction (CR) has a long history of experimentation in animals where it has also been seen to increase ROS antioxidant defense systems including superoxide dismutase, catalase, and glutathione peroxidase. (90)

In spite of improved availability of foods containing anti-carcinogenic phytonutrients and vitamins, many types of cancer have not declined as expected. This correlates to the overall calorie increase and overweight condition of our society, a condition which puts us in “constant feast” mode instead of the periodic fasting our ancestors previously experienced. (91) Many observers feel that our previous occasional fast, which would induce ketosis, was also beneficial for cancer control. It has also been hypothesized that some alternative cancer treatments, such as juice fasting or the use of Coley’s toxins, are effective primarily because they induce metabolic ketosis.

Additional Nutritional and Botanical Interventions

Although virtually any nutrient or herb can be considered in cancer treatment because of the multiple systems involved in same, only a relatively small handful of specific nutrients and botanicals have been well-studied and consistently proven to benefit the cancer patient. We will confine our discussion to those substances with a long history of use in human malignancy.

Nutritional Supplementation in the Treatment of Cancer

Supplements of proven utility in cancer treatment include:

I.) Vitamin C: long used for it’s dual function of immune up-regulation and direct toxicity to cancer cells, but doses sufficient to achieve the cytotoxic effect are unobtainable via the oral route. For this reason, IV vitamin C should be considered in cancer therapy. (92)

II.) Vitamin D3 (cholecalciferol): vitamin D deficiency is a known risk factor for cancer development.(93) D3 induces differentiation, inhibits angiogenesis (94, 95,96) and shows antitumor activity.(97,98,99) It may also up-regulate vitamin A receptors.(94) Vitamin D3 may serve to prevent metastatic bone disease in higher doses, perhaps because it is needed for normal calcification of bone matrix.

III.) Melatonin: a hormone produced by the pituitary gland which regulates sleep and circadian rhythms. Melatonin is a more potent antioxidant than glutathione or vitamin E (101). In vitro, it demonstrates anti-estrogen activity and immune stimulation. (100) Recent studies show that melatonin inhibits cell proliferation profoundly in vivo but only weakly in vitro. It is synergistic with IL-2 and increases the effectiveness of IL-2 treatment. (102)

IV.) CoQ10 (ubiquinone): this vitamin-like compound is involved in mitochondrial energy production. The heart is a high user of CoQ10 and many chemotherapeutic drugs deplete body stores of this nutrient. CoQ10 has been used successfully to reduce chemotherapy-induced cardio toxicity. In breast cancer patients, a dose of 90mg daily increases late stage survival dramatically. Three cases of complete remission have been documented at higher doses (300-400mg) per day. (103)

V.) Selenium: studies show that seleium interferes with the activity of p53 genes that promote the growth of cancer and induces apoptosis (104,105,106).

VI.) Tocotrienols: a member of the Vitamin E family, tocotrienols induce apoptosis and S-phase arrest (107,108) and inhibit proliferation. (109)

Botanical Considerations in Cancer Treatment

A HIGHLY SELECTIVE MATERIA MEDICA

Classified by action:

Natural Killer (NK) Cell Activation

Allium sativum

Astragalus

Echinacea spp.

Eleutherococcus senticosus

Panax ginseng

T-Cell Activation

Allium sativum

Astragalus

Echinacea spp.

Eleutherococcus

Anti-tumerogenic

Allium sativum

Berberine derivatives:

Hydrastis canadensis

Berberis aquifolia

B. vulgaris

Curcuma longa

Echinacea spp.

Stimulants of IgG & IgM Production

Panax ginseng

Anti-inflammatory

Ananas comosus

Curcuma longa

Fibrinolytic

Allium sativum

Ananas comosus

Macrophage Activation

Allium sativum

Aloe vera

Berberine derivatives:

Hydrastis canadensis

Berberis aquafolia

B. vulgaris

Coumarine derivatives:

Angelica sinensis-dong quai

Meliotus officinalis-sweet clover

Trifolium pratense- red clover

Echinacea spp.

Anti-metastatic

Ananas comosus

Larix spp.

modified citrus pectin (MCP)

Cytotoxic (IV administration)

Catharanthus roseus- periwinkle

vinblastin,vincristine,

vindesin,vinorelbine

Podophyllum peltatum-mayapple-podophyllotoxin

Taxus batacca- English yew- docetaxel

Taxotere®

Taxus brevifolia- Pacific yew- paclitaxel

Taxol®

Viscum album-mistletoe- Iscador®]

Materia Medica

Allium sativum (Liliaceae) – Garlic

As a food and a medicine, garlic comes closest to being a true panacea. Research has proved garlic’s immune-potentiating ability, including activation of NK and T-cells. (1,2,3,4.) Garlic is fibrinolytic, decreases platelet aggragation (5,6,7) and has been shown to have direct anti-tumor effects. 8,9,10. It is also a potent broad-spectrum antimicrobial, effective against alpha- and beta- Strep., E. coli., Klebsiella pneumonia, Mycobacterium, Salmonella, Staph. aureus, and Proteus spp. (17, 18, 19)

Aloe vera (Liliaceae) – Aloes

Acemannan, a water-soluable polysaccharide in Aloe vera, is a known immuno-stimulant (27,28) and anti-viral. (29) It’s mechanism of action is thought to be via stimulation of macrophage secretion of Tumor Necrosis Factor (TNF), interleukon, and interferon.

Ananas comosus (Bromeliaceae) – Pineapple (bromelain)

Bromelain is a sulfur-containing proteolytic enzyme from the stem of the pineapple plant. Other constituents include a non-proteolytic plasminogen activator, a peroxidase, and several protease inhibitors. (22,23)

Bromelain possesses significant anti-inflammatory activity by selective inhibition of pro-inflammatory prostaglandins. (16, 20) It also possesses fibrinolytic activity secondary to plasminogen activator (21) which may account for the antimetastatic properties seen in vivo. (24, 25, 26)

Astragalus membranaceus (Leguminosae) – Astragalus, Milk Vetch, Huang QI

Astragalus increases NK and T cell activity (11,12) in both normal and immunocompromised hosts.(13) It increases interferon production and is antibiotic against Shigella, Strep., Staph. and Diplococcus.(15)

Berberine derivatives:

Hydrastis Canadensis – (Ranunculaceae) – Goldenseal

Berberis aquafolia – (Berberidaceae) – Oregon Grape

Berberis vulgaris – (Berberidaceae) – Barberry

Berberine, an alkaloid derivative from various plants, has demonstrated significant antitumor effects with kill rates of 81% in vivo and 91% in vitro. This compares favorably to BCNU, a chemotherapeutic agent with a kill rate of 43% in vitro. (30)

Berberine sulfate also shows macrophage activation and cytostatic activity against tumor cells in vitro. (31) Berberine is well known for its broad spectrum antimicrobial activity (32,33,34) which is most effective in a neutral to alkaline medium. (35)

Courmarin derivatives:

Angelica sinensis – (Umbelliferaceae) – Dong quai

Metolium officinalis – Sweet clover

Trifolium pretense – (Leguminosae) – Red clover

Coumarin (1,2-benzopyrone) is a component of several medicinal plants that have been used historically in the treatment of cancer. Recent research has shown an immunomodulatory effect through activation of macrophages and monocytes. (39)

Curcuma longa – (Zingiberaceae) – Turmeric

Curcumin, a major component in turmeric, is a potent antioxidant and hepatoprotectant. It has been shown to inhibit cancer in all stages of development (initiation, promotion, and progression), (36) and provide symptom relief when used topically on external cancers. (37)

Anti-inflammatory effects are believed due to its ability stabilize lysosomal membranes and uncouple oxidative phosphorylation. At higher doses, curcumin stimulates endogenous corticoid release. (38)

Echinacea purpura, E. angustifolia (Compositae) – Purple coneflower

Echinacea is one of the most widely studied medicinal herbs, and its immune-potentiating effects are not in question.

Arabinogalactin, a purified polysaccharide from E. purpura, has been shown to activate macrophage cytotoxicity to tumor cells, increase interferon production, stimulate T-lymphocyte production and activity, enhance NK cell activity and increase levels of circulating neutrophils. (40, 41, 42,43)

Echinacea stimulates non-specific defense mechanisms including alternate complement pathway. (44) It is anti-tumerogenic in animal models. (45)

Eleutherococcus senticosis – (Araliaceae) – Siberian ginseng

Eleutherococcus has been shown to both elevate numbers and activate helper / inducer lymphocytes and NK cells. (46)

It has been revered in Russia as an adaptogen, and studies confirm that it normalizes numerous physical functions regardless of the direction of imbalance. (47)

Larix occidentalis, L. dahurica – (Pinaceae) – Larch

Larch is a deciduous conifer that contains an arabinogalactan similar to that in other “immune enhancing” herbs including Echinacea spp., Baptisia tinctora, and Curcuma longa.

Larch arabinogalactans have been shown to reduce the number of liver metastasis in multiple studies (48,49,50,51), perhaps by acting as a “reverse lectin” and blocking tumor binding sites. (52) A similar effect has been noted for Modified Citrus Pectin (MCP). (See below)

Panax ginseng – (Araliaceae) – Chinese or Korean ginseng

Ginsenosides, an active constituent in P. ginseng, have been shown to increase both the number and the activity of lymphocytes in healthy subjects. (53)

Large doses in lab animals (human equivalent of 500 -125,000 mg) for five days increased IgG and IgM formation by 50 and 100% respectively, and enhanced NK cell activity and interferon production. (54)

Ginseng has long been considered an adaptogenic herb, and recent research verifies that it increases resistance to physical and chemical stress. (55,56)

Modified Citrus Pectin (MCP)

Pectin, a high molecular-weight polysaccharide present in the cell wall of all plants, can be pH degraded to produce a modified (smaller) polysaccharide with anti-metastatic capabilities. (57) MCP appears to bind with galectins on cancer cell surfaces, inhibiting aggregation and adherence to normal cells (58) and offering anti-metastatic protection in animal models. (59,60,61)

In Summary

Much more is known about the management of cancer, including how to evoke durable remissions and even cure, than is generally used or discussed in conventional medicine. Perhaps this is because some of the most powerful and proven therapies do not require drugs or invasive intervention.

“Those who battle nature as their enemy will lose; those who use nature to battle their enemy will win.” —Mark Ziemann, R.N.

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