Dr. Myatt’s HealthBeat Newsletter

April 14, 2006

In this issue:

Vitamin-less Vegetables: The New Nutrient Deficiency. Vegetables and some fruits contain nutrients critical to good health. Current government recommendations suggest that a minimum of 5-9 servings should be eaten daily to prevent disease, but many scientists feel this number should be increased to 10-18 servings. Find out why we need to eat so many veggies (it’s a scandal!), and how you can achieve this goal without turning into a wabbit!

Powerful Cancer-fighting Herb that Drug Companies are Rushing to Imitate. You probably have some in your spice cabinet right now. Use more of it, and you can hedge your bet against cancer, arthritis and blood clots.

The Healing Power of Flowers. Humans spend much time and money cultivating flowers. Science has finally cracked the code on our fascination with these delightful gifts of nature. PLUS: it’s not too late to send flowers for Easter. You’ll want to lavish them on friends and family once you read the studies!

Health Freedom Alert: Bio-Identical Hormone Therapy Under Attack. Bio-identical (natural) hormone replacement therapy (nHRT) is far safer than synthetic and horse-urine hormones used in conventional medicine. It has helped thousands if not hundreds of thousands of women and men over the last several decades. Now, the makers of Premarin© and Prempro© (the dangerous, un-natural hormones) has petitioned the FDA to outlaw our right to prescribe these custom-formulated hormones. Act today to preserve this important health freedom!

Wellness Club Website Wins Award. Dr. Myatt’s Wellness Club website was nominated, reviewed, and awarded the “A Better Way Award” for noteworthy contribution to the Natural Health Community. You’ll see us sporting our award logo on the left side of our pages. Interestingly, the logo for the award is a big, red apple—- the same as our Wellness Club logo!

Dr. Myatt and Nurse Mark to Speak in Phoenix. The~Z~Team (Dr. Myatt-Ziemann and Mark Ziemann, R.N.) will be speaking in Phoenix the end of April to both public and medical audiences. The public presentation, titled ADD/ADHD in Children: are there Really Alternatives to Ritalin and Prozac? Is free and open to the public. The second presentation, Nutritional and Botanical Considerations in Cancer Treatment: 2006 Update, will be presented to physicians at the semi-annual AZNMA Medical Conference.

The Shaman’s Lesson of Worth. Think you can’t afford alternative health care? I have people on a daily basis asking me to do pro bono medical consultations. Find out what I learned from an Indian Shaman in my first year of medical practice that makes me say “no” every time to these requests for free services.

Do you have a specific health question? Visit Dr. Myatt’s Wellness Club website and find recommendations for over 100 medical conditions. If you want personalized medical attention, please consider a telephone consultation with Dr. Myatt.

Vitamin D

The Sunshine Vitamin For Healthy Bones, Teeth, and Cancer Prevention

Vitamin D increases calcium absorption. Deficiencies of Vitamin D are associated with infertility, cancer, osteoporosis, rheumatic pains, and dental disease

It is known as the SUNSHINE vitamin because exposure to sunshine, even as little as 10 minutes per day, promotes the body’s natural production of Vitamin D. Those living in northern climates where sunshine is limited or in southern areas who shield themselves from the sun with clothing or sunscreen can easily become deficient in Vitamin D.

Dr. Braverman says about Vitamin D:

New research is showing the anti inflammatory benefits of Vit D. It has been shown to decrease NK cell activity, as well as alter the TH1/TH2 cytokine ratio in favor of the anti inflammatory response by lowering TH1 and increasing TH2.  Its effects are very similar to the TH2 cytokine called IL-10 one of the most important TH2 cytokines produced for the maintenance of pregnancy.  It is the TH2 cytokine we measure with our TH1/TH2 ratio. We recommend patients that require this therapy take between 2000 and 4000 IU /day.  We have started screening our patients for what is turning out to be a common vitamin deficiency in this country.

Dietary sources of vitamin D include: fish liver oil and egg yolk.

More recently, higher intakes of vitamin D have been shown to protect the body from cancer, especially prostate and breast cancer. Many authorities are recommending that the recommended adult daily dose should be raised from 400 IU to 1,000 IU. Doses of 1,000-6,000 are not only safe, they may be needed for disease prevention.

Maxi Multi contains 800 IU of Vitamin D per daily serving.

NOTE: Do not use more than 10,000 IU per day without medical supervision because Vitamin D is a fat-soluble vitamin. Although vitamin D can store in the liver and become toxic, these toxicities were seen in people consuming 30,000IU or more (20 times the recommended dose!) for months. Vitamin D is much safer than we have previously been led to believe.

Suggested dose: Daily adult dose range: 800-2,000 IU. Doses as high as 10,000 IU may be needed to normalize vitamin D levels.

Vitamin D 5000 – Product # 288  (250 Capsules) $21.95

Each (one) capsule contains: Vitamin D3 (cholecalciferol) 5000 IU.

References:

Please see a full list of references at this special report:  Vitamin D Special Report

Design Your Own Optimal Health / Anti-Aging Supplement Program

Natural Support To Keep You In The Peak Of Health For Years To Come

Step 1: Optimal Dose Multivitamins & Minerals

Optimal (not just minimal) doses of vitamins, minerals and antioxidants should be the foundation of every good health program. For information about optimal daily adult doses of nutrients, refer to the vitamin/mineral chart here.

Dr. Myatt’s Maxi Multi delivers optimal daily doses of vitamins, minerals and trace minerals in a single formula. Other possible combinations of formulas based on age and sex can be found here: Which Formulas Are Right For You?

If you take only one thing, make it an optimal potency multiple vitamin / mineral / trace mineral / antioxidant formula such as Maxi Multi or equivalent combination.

[Note: To obtain the equivalent of Maxi Multi’s, most people need to take the following: I.) High quality multiple vitamin / mineral formula II.) B complex vitamins III.) Additional antioxidant formula IV.) Calcium / magnesium / boron.]

Step 2: Phyto-nutrients

Plants contain hundreds of non-vitamin/non-mineral substances known as “phytonutrients.” (Phyto=plant). Although not absolutely essential to to life like vitamins and minerals are, these plant-derived nutrients never-the-less perform many important functions. Phytonutrients act as potent antioxidants, detoxifiers, oxygenators and anti-mutagenics. (Preventing cancerous changes in cells). The typical American diet is far too low in produce, so plant-derived nutrients are often lacking. Supplementing flavonoid-rich herbs is good “health insurance.” Maxi Greens provides a broad spectrum of phytonutrients in a single formula OR use other flavonoid-rich herbs singularly or in combination.

Step 3: Organ System or Condition-Specific Protocols

If you have a medical diagnosis, you may choose to use a supplement protocol that has been proven useful for your condition. You can look up medical conditions in the “Disease” Knowledge Search box on the upper right hand corner of every page on this website. If you do not have a diagnosis OR if you wish to practice preventive medicine, follow the “Health Priority Protocols” for any organ system that scored “high” on the Health Priority Self-Evaluation. The Health Priority Evaluation can be found on page 6-8 of the Holistic Health Handbook.

Step 4: Hormones

Hormones are potent “biochemical messengers” that control virtually every aspect of physical function. Many hormones, including sex hormones (DHEA, estrogens, progestins, testosterone), neurotransmitters (serotonin, dopamine) and melatonin decline with age. It is believed that the aging process can be slowed or countered by maintaining more youthful levels of these hormones.

Because the hormonal “milieu” is a complicated mix, I recommend hormone testing when available (as it is for the sex hormones) before beginning replacement therapy.

Additional Measures to Consider:

Cancer Prevention Protocol

1.) Take optimal daily doses of vitamins and minerals. (Maxi Multi or equivalent).
2.) Take additional flavonoid-rich herbs (Maxi Greens or equivalent).
3.) Omega-3 Essential Fatty Acids: fish oil (best) or flax oil OR 2 TBS. or more ground flax seed.
4.) Hormone Balancing as indicated by the results of a hormone profile.
5.) Cancer-prevention “extras” (if not included elsewhere in your program)

Use any or all:

Click here for Advice about Your Anti-Aging / Longevity Protocol

Q & A About Nutritional Supplements

Q: It seems strange to take so many supplements to stay healthy. Can’t I just get my nutrients from a good diet?

A: Theoretically, yes. Realistically, no. You need supplements to ensure that there are no “gaps” in your nutrient intake. And while it may seem “strange” to take supplements, consider how strange our eating behaviors have become.

We don’t eat fresh fruits and vegetables just picked from the vine; we eat produce that was grown with multiple pesticides and insecticides, then shipped long distances and kept in cold storage. Instead of fresh produce, we may be eating an apple that was picked 18 months ago. Nutrients are lost by the hour when produce is picked.

We no longer eat whole grain bread from freshly milled grain, with the germ (which contains vitamin E), and bran (which contains fiber and B complex vitamins) intact. Instead, our flour has been processed, all nutrients removed, bleached, chlorinated, baked into bread with preservatives added, then “enriched” with a few token nutrients.

Do you drink milk for the calcium? Or eat cheese? Our cattle are fattened by using human sex hormones and growth hormones to stimulate milk production and fatten them for beef. Those hormones are in the flesh and milk, and then passed on to us. High levels of dioxin are now found in cattle, presumably because this outlawed environmental toxin is making it’s way up the food chain.

I could go on, but what’s the point? Even if you consistently make every effort to eat healthfully, unless you raise all of your own food and eat it fresh, you are not obtaining the necessary nutrients from diet. Few people I know eat this way.

Numerous studies have demonstrated the protective value of obtaining target doses of various nutrients. Even a single nutrient deficiency can cause a whole “domino effect” of health problems, since “everything is connected to everything” in the body. Why take chances? Taking Maxi Multi is inexpensive health insurance.

Q: The recommended dose for Maxi Multi is 9 caps per day. I take a one-per day multi vitamin now. Why does your formula require so many capsules for a full day’s dose?

A: Because optimal doses of nutrients do not fit into one capsule or tablet.

Q: I have been taking vitamins from the health food store and I feel fine. Should I keep taking these, or switch to Dr.Myatt’s Maxi Multi’s?

A: Switch to Maxi Multi! Are you certain that your multiple contains optimal doses of all nutrients? Are you certain that it was manufactured with the highest quality raw materials? Verified by independent laboratory testing as well as stringent in-house testing? Does the company use the most efficacious form of each individual nutrient? Do they include important (but often overlooked) trace minerals such as molybdenum, vanadium and boron? Do they continually update the formula to reflect new discoveries in the field of nutritional medicine? Do they have me-”The Dragon Lady”- or someone just like me, watching every aspect of quality, purity, and formulation? If you want to be sure that you are getting all the nutrients your body needs on a daily basis, in the purest, most potent, optimal doses, take Maxi Multi.

Q: I take Maxi Multi’s every day. Do I need to take other supplements?

A: That depends. If you are in good health, have no medical problems, and follow the “Golden Rules of Good Health” at least 90% of the time, Maxi Multi’s may be all you need.

If you have already-existing health problems, do not follow good health practices on a regular basis, or want to do more to prevent problems, then additional supplementation is in order.

Maxi Multi’s provide a solid foundation for your good health program. They are inexpensive “health insurance” that will protect you from numerous deficiency-related disease, dietary imbalances, and environmental toxins. Consider Maxi Multi’s the starting place for your supplement protocol.

Every “protocol” listed here is built on a foundation of Maxi Multi’s or the equivalent. If you are not getting the “foundation,” additional supplementation will be far less beneficial.

Remember, if you only take one nutritional supplement, Maxi Multi should be The One.

ESSENTIAL FATTY ACIDS (EFA)

An Explanation Of These “Must-Have” Nutrients

Essential Fatty Acids (EFA’s) are fats required by the body that must be supplied by diet because the body cannot manufacture them, hence the term “essential.” These fats are the raw material for the production of prostaglandins (local-acting, hormone-like substances) in the body.

Some fats eventually become inflammatory prostaglandins. These inflammatory prostaglandins contribute to generalized inflammation and blood platelet “stickiness.” Inflammatory prostaglandins play an important role in the development of arthritis, rheumatoid arthritis, hardening of the arteries (atherosclerosis), stroke, heart disease and cancer. They may also contribute to pain and generalized inflammation.

In contrast, other fats become anti-inflammatory prostaglandins. This type of prostaglandin relieves painful inflammation, improves blood flow, and reduces the risk of heart disease, stroke, cancer and autoimmune disease.

Omega-6 fatty acids produce inflammatory prostaglandins almost exclusively. Many vegetable oils are Omega-6 oils.

The typical American diet is much higher in inflammatory fats than anti-inflammatory fats.

Glossary of Fats

Omega-3 Oils are derived primarily from fish oil and flax seeds. These essential fatty acids are anti-inflammatoryand have a positive effect on cardiovascular disease, including high cholesterol and high blood pressure, allergic and inflammatory conditions (including psoriasis and eczema), autoimmune diseases, cancer, neurological disease, menopause, general health enhancement. Supplementation with Omega-3 Essential Fatty Acids can help “tip the scales” in favor of anti-inflammation.

Omega-6 Oils are found in evening primrose, black current, borage and a number of vegetable oils. Although supplementation is popular, these oils are necessary only in very small amounts. Excess Omega-6 oils increase arachadonic acid levels (an inflammatory substance). Only diabetics usually need to supplement very small doses of these oils. (Less than 500mg/day).

Omega-9 Oils are found in olive and canola oils. These oils are neutral, producing neither inflammation nor anti-inflammation. Extra virgin olive oil is a good choice for salad dressings & stir-frying food because it is expressed mechanically, without the use of chemicals.

Omega-3 Essential Fatty Acid Deficiency is a common problem in the average American diet, and supplementation with Omega-3 Essential Fatty Acids is almost always indicated. Find the best dietary sources of Essential Fatty Acids here.

Nutritional and Botanical Considerations in the Systemic Treatment of Cancer: 2006, 2010 Update

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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19.) Elnima, E.I. et al.: The antimicrobial activity of garlic and onion extracts. Pharmazie 38:747-48, 1983.

20.) Taussig, S., Batkin, S.: Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharm 22:191-203, 1988.

21.) Felton, G.E.: Fibrinolytic and antithrombotic action of bromelain may eliminate thrombosis in heart patients. Med Hypothesis, 6: 1123-33, 1980.

22.) Felton, G.E.: Does kinin released by pineapple stem bromelain stimulate production of prostaglandin E1-like compounds? Hawaii Med J 36:39-47, 1977.

23.) Taussig SJ.: The mechanism of the physiological action of bromelain. Med Hypothesis 6:99-104, 1980.

24.) Batkin, S., et al.: Modulation of pulmonary metastasis (Lewis lung carcinoma) by bromelain, an extract of the pineapple stam (Ananas comosus). Letter. Cancer Invest 6(2):241-242, 1988.

25.) Goldstein N., et al.: Bromelain as a skin cancer preventive in hairless mice. Hawaii Med J, 34:91-4, 1975.

26.) Gerard G., Therapeutique anti-cancreuse et bromelaines. Agressologie 3:261-274, 1972. (In French).

27.) Sheets, MA., Unger, BA., Giggleman GF Jr., Tizard, IR.: Studies of the effect of acemannan on retrovirus infections: Clinical stabilization of feline leukemia virus-infected cats. Mol Biother 3(1):41-45, 1991.

28.) Peng, SY., Norman J., Curtin G., et al.: Decreased mortality of Norman murine sarcoma in mice treated with the immunomodulator, acemannan. Mol Biother 3(2): 79-87, 1991.

29.) Kahlon, J.B., et al.: In vitro evaluation of the synergistic antiviral effects of acemannan in combination with azidothymidine and acyclovir. Mol Biother 3:214-23, 1991.

30.) Rong-xun Z., et al.: Laboratory studies of berberine used alone and in combination with 1,3bis (2-chloroethyl)-1-nitrosurea to treat malignant brain tumors. Chinese Med J 103(8):658-65, 1990.

31.) Kumazawa Y., et al.: Activation of peritoneal macrophages by berberine-type alkaloids in terms of induction of cytostatic activity. Int J Immunopharmacol 6(6):587-92, 1984.

32.) Hahn, F.E., Ciak, J.: Berberine. Antibiotics 3:577-88, 1976.

33.) Ghosh, A.K.: effect of berberine chloride on leishmania donovani. Ind J Med Res 78:407-16, 1983.

34.) Subbaiah, T.V., Amin, A.H.: Effect of berberine sulfate on E. histolytica. Nature 215:527-28, 1967.

35.) Amin, A.H., Subbaiah, T.V., and Abbasi, K.M.: Berberine sulfate: Antimicrobial activity, bioassay, and mode of action. Can J Microbiol 15:1067-76. 1969.

36.) Nagabhushan, M., Bhide, SV.: Curcumin as an inhibitor of cancer. J Am Col Nutr 11(2):192-8, 1992.

37.) Kuttan, R., Sudheeran PC., Josep CD.: Turmeric and curcumin as topical agents in cancer therapy. Tumori (Italy) 73:29-31, 1987.

38.) Srivastava R, Srimal, RC.: Modification of certain inflammation-induced biochemical changes by curcumin. Ind J Med Res 81:215-223, 1985.

40.) Luettig, B., et al.: Macrophage activation by the polysaccharide arabinogalactan isolated from plant cell cultures of Echinacea purpurea. J Natl Cancer Inst 81(9):669-75, 1989.

41.) Wagner, V.., Proksch, A., Zeitschrift Feur Agnewande Phytotherapie (German) 2(5):166-168, 171, 1981.

42.) Wagner, V., Proksch,A., Riess-Maurer,I., et al.: Immunostimulatin polysaccharides (heteroglycane) of higher plants: Preliminary communications. Arzneim Forsch 34:659-60, 1984.

43.) Mose, J.: Effect of echinacin on phagocytosis and natural killer cells. Med Welt 34:1463-67,1983.

44.) Vomel,V.: Influence of a non-specific immune stimulant on phagocytosis of erythrocytes and ink by the reticuloendothelial system of isolated perfused rat livers of different ages. Arzneim Forsch 34:691-95, 1984.

45.) Bauer, R., Jurcic, K., Puhlmann,J., Wagner, H.: Immunological in vivo and in vitro examinations of Echinacea extracts. Arzneim Forsch 38:276-281, 1988.

46.) Bohn,B., Nebe, C.T., Birr, C.: Flow-cytometric studies with Eleutherococcus senticosus extracts as an immunomodulatory agent. Arzneim-Forsch 37:1193-96, 1987.

47.) Pizzorno, J.E., Murray, M.T.: Eleutherococcus senticosus: A Textbook of Natural Medicine, Bastyr University Publications, Seattle, WA, 1995.

48.) Hagmar, B., Ryd, W., Skomedal, H.: Arabinogalactan blockade of experimental metastasis to liver by murine hepatoma. Invasion Metastasis 11(6):348-55, 1991.

49.) Uhlenbruck G., Beuth J., Roszkowski W., et al.: Prevention of experimental liver metastasis by arabinogalactan. Naturwissenschaften 73(10)626-7, Oct. 1986.

50.) Beuth J., Ko HL., Oette K., et al.: Inhibition of liver metastasis in mice by blocking hepatocyte lectins with arabinogalactan infusions and D-galactose. J cancer Res Clin Oncol 113(1): 51-5,1987.

51.) Beuth J., Ko HL., et al.: Inhibition of liver tumor cell colonization in two animal tumor models by lectin blocking with D-galactose or arabinogalacan. Clin Exp Metastasis 6(2):115-20, Mar-Apr 1988.

52.) D’Adamo, P.: Larch arabinogalactan. J Nat Med 6(1):33-36, 1996.

53.) Scaglione, F., et al.: Immunomodulatory effects of two extracts of Panax ginseng. Drugs Exp Clin Res 16:537-42, 1990.

54.) Jie, Y.H., Cammisuli,S., Baggiolini, M.: Immunomodulatory effects of Panax ginseng C.A. Meyer in the mouse. Agents Actions 15: 386-91, 1984.

55.) Bahrke M.S., Morgan W.P.: Evaluation of the ergogenic properties of ginseng. Sports Med 18: 229-48, 1994.

56.) Brekhman I., Dardymov I.V.: Pharmacological investigation of glycosides from ginseng and eleutherococcus. Lloydia 32:46-51, 1969.

57.) Kidd, P.M.: A new approach to metastatic cancer prevention: modified citrus pectin (MCP), a unique pectin that blocks cell surface lectins. Alt Med Rev 1(1): 4-10, 1996.

58.) Sharon N., Lis H.: Lectins as cell recognition molecules. Science 246:227-34, 1989.

59.) Platt D., Raz A.: Modulation of the lung colonization of B16-F1 melanoma cells by citrus pectin. J Natl Cancer Inst 84:438-442, 1992.

60.) Pienta KJ., et al.: Inhibition of spontaneous metastasis in a rat prostate cancer model by oral administration of modified citrus pectin. J Natl Cancer Inst 87:348-53, 1995.

61.) Raz, A., Lotan R.: Endogenous galactoside-binding lectins: a new class of functional cell surface molecules related to metastasis. Cancer Metastasis Rev 6:433-52, 1987.

Consultations With Dr. Dana Myatt

Help Yourself To Good Health

Notice To New Patients:

Because of Dr. Myatt’s reputation of being the doctor to call when conventional medicine gives up she has been inundated with a number of extremely complicated patients.

In order that she may continue to provide all her patients the high levels of care and attention that they have come to rely upon she is accepting only very select new patients.

In order to determine suitability to be added to her caseload Dr. Myatt is requiring all those who wish to be taken on as new patients to first speak with her in a Brief Telephone Consultation.

DANA MYATT, N.M.D.

Member: American Association of Naturopathic Physicians (eligible)
President: ECAFH Foundation, Inc. (Exploring Complementary Answers for Health)
Author: A Physicians Diary
Professor: Atlantic University
Graduate: National College of Naturopathic Medicine

How May I Help You? Herbs Homeopathy Nutritional Evaluations Lifestyle Counseling Chinese Medicine Edgar Cayce Remedies Health Optimization Immune Enhancement Detoxification and Fasting Stress Reduction Health Education Weight Management

 

Special Programs

  • Executive Wellness & Longevity
  • Cardiovascular disease prevention and reversal / high cholesterol reversal
  • Overweight/obesity
  • CANCER prevention/options
  • Digestive difficulties and parasites
  • Allergies and hypersensitivities
  • Depression and anxiety
  • Viral Syndromes including HIV, herpes, Epstein Barr (EBV), hepatitis
  • Infertility (male and female)
  • Athletic performance

DR. DANA MYATT
Help Yourself to Health

Click Here To Learn Why You Should Consult Dr. Myatt

click here to see Dr. Myatt’s telephone consult brochure

call 1-800-DRMYATT (1-800-376-9288)

Please also see: How Our Office Handles Insurance

Do Doctors Still Make House Calls?

Dr. Myatt And Nurse Mark Make “The Ultimate House Calls”!

Many of our private practice patents and Wellness Club Customers know that Dr. Myatt travels often to speak, teach, and lecture. When her travels bring her to areas where her patients live she is happy to schedule them for an in-person consultation, including examination and other therapeutic treatments. Patients may be seen in Dr. Myatt’s Wellness Club coach or even in the comfort of their own home. When visits can be scheduled to coincide with Dr. Myatt’s travel itinerary her customary consultation fees apply.

Your Own Private Naturopathic Doctor And Nurse – In Attendance:

For those who need the undivided attention of this unique doctor and nurse team, Dr. Myatt and Nurse Mark can travel to your location where they will attend to your holistic health needs 24/7 if need be. This may include not only intensive care for the patient, it may include teaching for family members and caregivers or for staff such as personal chefs, personal assistants, housekeepers, or security staff.

You can be assured of absolute, inviolate confidentiality and respect for your privacy when working with Dr. Myatt and Nurse Mark.

This is a unique and specialized service and it is not inexpensive. Not all patients will qualify for or benefit from this intensive in-home naturopathic medical care. Please contact Dr. Myatt for cost and availability and to determine your suitability for this ultimate health-restorative opportunity.

Is your situation more urgent?

Do you need Dr. Myatt and Nurse Mark to attend you more quickly than is possible with road travel? (for road travel figure 500 miles per day from northern Arizona to your location)

Dr. Myatt will not travel by commercial (public) air carrier. She will consent to travel by private business aircraft and there is an airfield near her location that will accommodate this class of aircraft. (KTYL) Contact The Wellness Club to discuss this option.

Dr Myatt can also arrange to travel to your location by private plane. Nurse Mark is a licensed Private Pilot and their airplane allows them to reach you quickly and discretely. Requirements for visitations of this kind will include a destination airport with adequate runways and secure tie-downs and available fuel, appropriate transportation arrangements on arrival and during the visit, and appropriate accomodations for Dr. Myatt and Nurse Mark while on location.

Piper Warrior II Private Airplane
Dr. Myatt and Nurse Mark can be at your side quickly if need be. Click on the picture above for more information about their aircraft.


Dr. Myatt’s Wellness Club Coach is 36 feet in length. She maintains contact with her patients and the internet via 2-way satellite. When in location she requires electrical service for her communications: 20 amps minimum.

Brief Consultations

Brief Consultations by telephone are available between 9 AM and 5 PM, Tuesday through Friday, Arizona time. When you checkout please tell us what times and dates would be best for your consultation – we will make every effort to accommodate your needs, subject to prior scheduling commitments. Please be sure that we have both a valid email and telephone number so we can contact you to arrange your appointment.

Please Note: Be sure that you are available at the telephone number you provide, at the time you have arranged, when Dr. Myatt calls you – there are no refunds for missed appointments!

In the very unlikely event that a medical emergency prevents Dr. Myatt from calling at your appointment time, you will be offered a full refund or a rescheduled appointment – your choice.

DO NOT send Dr. Myatt lab reports, medical records or summaries, or any other medical information unless you are booking a New Patient Visit Consultation! Any medical information that is received unsolicited will be treated as confidential medical records and will be destroyed immediately.

Medical records and other documentation can be sent to:

Dr. Myatts Wellness Club
Attn: Medical Records
PO Box 900
Snowflake, AZ 85937

It is of no benefit to send via “overnight” courier – USPS Priority Mail provides timely and inexpensive delivery to our location – usually as quickly as any “overnight” courier!

CANCER

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.
      • 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)

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.

 

CANCER PREVENTION

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

 


References

Body Weight (BMI) and Cancer

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Super Foods

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11.) Geller J, Sionit L, Partido C, et al. Genistein inhibits the growth of human-patient BPH and prostate cancer in histoculture. Prostate 1998;34:75–9.

Smoking, Alcohol and Cancer Risk

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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.

Drinking Water and Cancer Risk

1.) Richardson SD, Plewa MJ, Wagner ED, Schoeny R, Demarini DM. Occurrence, genotoxicity, and carcinogenicity of regulated and emerging disinfection by-products in drinking water: a review and roadmap for research. Mutat Res. 2007 Nov-Dec;636(1-3):178-242. Epub 2007 Sep 12.
2.) Kasim K, Levallois P, Johnson KC, Abdous B, Auger P; Canadian Cancer Registries Epidemiology Research Group. Chlorination disinfection by-products in drinking water and the risk of adult leukemia in Canada. Am J Epidemiol. 2006 Jan 15;163(2):116-26. Epub 2005 Nov 30.
3.) Do MT, Birkett NJ, Johnson KC, Krewski D, Villeneuve P; Canadian Cancer Registries Epidemiology Research Group. Chlorination disinfection by-products and pancreatic cancer risk.
Environ Health Perspect. 2005 Apr;113(4):418-24.
4.) Cancer Causes Control. 1996 Nov;7(6):596-604. Drinking water source and chlorination byproducts in Iowa. III. Risk of brain cancer. Am J Epidemiol. 1999 Sep 15;150(6):552-60.
5.) Wigle DT. Safe drinking water: a public health challenge. Chronic Dis Can. 1998;19(3):103-7. Review.
6.) Cantor KP, Lynch CF, Hildesheim ME, Dosemeci M, Lubin J, Alavanja M, Craun G.Drinking water source and chlorination byproducts. I. Risk of bladder cancer. Epidemiology. 1998 Jan;9(1):21-8.
7.) King WD, Marrett LD. Case-control study of bladder cancer and chlorination by-products in treated water (Ontario, Canada). Cancer Causes Control. 1996 Nov;7(6):596-604.

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.

Emotional Hygiene and The immune System

1.) Chandrashekara S, Jayashree K, Veeranna HB, Vadiraj HS, Ramesh MN, Shobha A, Sarvanan Y, Vikram YK. Effects of anxiety on TNF-alpha levels during psychological stress. J Psychosom Res. 2007 Jul;63(1):65-9.
2.) Witek-Janusek L, Gabram S, Mathews HL.Psychologic stress, reduced NK cell activity, and cytokine dysregulation in women experiencing diagnostic breast biopsy. Psychoneuroendocrinology. 2007 Jan;32(1):22-35. Epub 2006 Nov 7.
3.) Di Donato A, Di Giampaolo L, Reale M, Dadorante V, Alparone F, Stocchi M, Fattorini E, Di Gioacchino M, Magrini A, Boscolo P. Effect of occupational stress and anxiety on natural killer lymphocyte activity of men and women employed in a university. Int J Immunopathol Pharmacol. 2006 Oct-Dec;19(4 Suppl):79-84.
4.) Barak Y. The immune system and happiness. Autoimmun Rev. 2006 Oct;5(8):523-7. Epub 2006 Mar 21.
5.) Ickovics JR, Milan S, Boland R, Schoenbaum E, Schuman P, Vlahov D; HIV Epidemiology Research Study (HERS) Group.Psychological resources protect health: 5-year survival and immune function among HIV-infected women from four US cities. AIDS. 2006 Sep 11;20(14):1851-60.
6.) Rosenkranz MA, Jackson DC, Dalton KM, Dolski I, Ryff CD, Singer BH, Muller D, Kalin NH, Davidson RJ. Affective style and in vivo immune response: neurobehavioral mechanisms. Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):11148-52. Epub 2003 Sep 5.

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.

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.

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.

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.

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.

Nutritional and Botanical Considerations in the Systemic Treatment of Cancer: 2010 Update

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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