Cytokines

A Simplified Look At Messenger Molecules

(or… Don’t Shoot the Messenger!)

Let’s get something straight right up front: cytokynes are not a toxin or a disease or something bad to be stamped out. They are just messengers.

Cytokines are not the disease or infection or insult, they are the message that is created by white blood cells (lymphocytes and macrophages), epithelial cells (cells that line internal tissues) and by other cells in lesser degrees, in response to some insult like a bacteria, virus or other infection. They can cause inflammation and are also created in response to inflammation.

Cytokines are the way that cells in distress call other cells for help — like an S.O.S.

When our immune system is fighting pathogens, cytokines call immune cells such as T-cells and macrophages to travel to the site of the infection.

Measuring cytokines gives us an indication of what is going on that would cause our cells to be calling for help.

When we talk about lowering inflammatory cytokines what we really should be talking about is addressing the cause of the inflammation so that cytokine-producing cells no longer feel the need to send out “help me!” messages.

Cytokines work on a “negative feedback” system. When there is a stimulus (a reason for cells to need help), cytokines are produced. The greater the stimulus, the more cytokines are produced. If the stimulus becomes less (when the infection heals or the inflammation subsides), cytokine production decreases because less are needed. Like the gas pedal on your car, to go faster you press harder – if you remove your foot (removing the stimulus) the engine slows down and the car stops.

Occasionally the cytokine response can become unbalanced, entering a sort of positive feedback loop which can easily get out of control – imagine if your car’s gas pedal worked the other way, where you had to keep it pressed down to stop! This has been termed a “cytokine storm” and is a serious medical emergency that can result in organ damage and even death. It is one reason for the deaths of people with otherwise healthy immune systems in pandemics such as the Spanish Flu of 1918 or the more recent Bird Flu and Swine Flu outbreaks.

There are three broad categories of cytokines – they can be grouped according to what they do, though there is also a lot of redundancy and “cross training” going on with cytokines.

First, there are Cytokines involved in innate (as in “born with it”) immunity and inflammation. Most of these cytokines are made by macrophages (important for removing pathogens), mast cells (important to inflammation) and endothelial cells (the cells that line our blood vessels and lymphatic system).

Major players here include:

  • TNF (tumor necrosis factor) and interleukin-1 (IL-1) help to activate endothelial cells.
  • Chemokines serve to attract different kinds of leukocytes (infection-fighting white blood cells)
  • IL-12 and interferon-gamma (IFN-y) are more involved in chronic inflammation.

Then there are cytokines involved in adaptive (as in “acquired in response to an infection or vaccination”) immunity. Most of these cytokines are made by our T helper cells (T cells are a kind of lymphocyte that matures in our thymus gland – hence the ‘T‘).

There are 2 main kinds of T Helper cells:

  • Th1 cells: Type 1 helper T cells make pro-inflammatory cytokines like IFN-y, IL-2, and TNF. These cells are involved in cell-mediated immunity and the cytokines produced by them stimulate the breakdown of microbial pathogens. Several chronic inflammatory diseases like multiple sclerosis, diabetes, and rheumatoid arthritis are considered Th1 dominant diseases.
  • Th2 cells: Type 2 helper T cells produce the cytokines IL-4, IL-5, IL-9, IL-10, and IL-13. Th2 cells are involved in allergy responses. Cytokines like IL-4 stimulate antibodies directed at extracellular parasites and at viruses. IL-5 stimulates eosinophil (a kind of white blood cell) responses, also part of the immune response toward large extracellular parasites. Allergy is considered to be Th2 dominant condition.

While Th1 cells are generally thought to produce inflammatory cytokines and Th2 cells are thought to produce inflammation-mediating cytokines, as you can see here there is “crossover.”

  • IL-2 and IL-4 cytokines tell lymphocytes to proliferate and differentiate (that means to grow, mature, and take on a specialized function).
  • IFN-gamma and IL-5 cytokines send messages that activate other cells.

Then there are cytokines involved in hematopoiesis – a fancy word that means “building new blood cells” – either oxygen-carrying red blood cells or infection-fighting white blood cells. Cells that make these cytokines include endothelial cells, macrophages, and other cells in our immune system. An example of this are colony-stimulating factors like G-CSF (granulocyte-colony stimulating factor) which causes hematopoietic cells to grow.

These are just a few of the more broad classes of cytokines – there are hundreds of these chemical messengers, each with a unique purpose and job to do.

Some of the ones we hear about most often are:

  • TNFa or Tumor Necrosis Factor alpha. While the name sounds ominous, TNF is a vital player in our response to infection. Its primary role is the regulation of immune system cells. TNF is able to induce fever, cause cell death, cause cachexia, initiate inflammation and to inhibit tumor growth and viral replication in response to sepsis or infection.
  • Interleukin 6 (IL-6) is an cytokine that acts as both a pro-inflammatory cytokine and an anti-inflammatory myokine (produced from muscle cells). [could this get any more confusing?] While IL-6 serves to stimulate the inflammatory and auto-immune processes in many diseases it also is anti-inflammatory in that it moderates or mediates inflammation by inhibiting TNF-alpha and IL-1, and by activating other interleukins such as IL-10.
  • Interferon gamma (IFNγ or type II interferon) is a cytokine that is critical for both innate and adaptive immunity against viral and some bacterial and protozoal infections. IFNγ activates macrophages. If IFNγ becomes uncontrolled it can be associated with a number of auto-inflammatory and autoimmune diseases. Its importance in the immune system comes from its ability to inhibit viruses directly, and most importantly from its stimulating and modulating effects on immunity. IFNγ is produced mainly by natural killer (NK) and natural killer T (NKT) cells.
  • Interleukin 10 (IL-10) is an anti-inflammatory cytokine. IL-10 inhibits production of pro-inflammatory cytokines like as IFN-γ, IL-2, IL-3, TNFa and GM-CSF made by cells such as macrophages and T-cells. IL-10 is important for counteracting hyperactive immune responses that can occur with over-stimulation of pro-inflammatory cytokines.

Importantly, we need to remember that many of the inflammatory cytokines are induced by oxidative stress – meaning that antioxidants play an important role in reducing the production of inflammatory cytokines.

Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen that form when cells metabolize oxygen. In normal amounts ROS have important roles in cellular health. In times of stress (exposure to pathogens, toxins, UV or heat, ionizing radiation, etc.), ROS levels may greatly increase which can damage cells. This is known as oxidative stress and ROS are sometimes called “free radicals.”

Also remember that cytokines themselves trigger the release of other cytokines leading to increased oxidative stress. This makes them important in chronic inflammation, as well as other immune responses such as fever.

So, when your doctor presents you with your lab results and says “you have some high cytokines – we need to get those down,” he really means that there are some stresses going on – infection, chronic inflammation, allergy, oxidative stress, toxicity – that are being shown to him by the cytokines that can be measured. These stresses — the cause of elevated cytokines — are what must be dealt with in order to “bring down” the high cytokines, not the other way around. “Bringing down” high cytokines will not correct the insult (infection, toxicity, inflammation, etc.) that is causing the problem in the first place.

Maxi Flavone is formulated to “bring down” high cytokines – but not in a way that a drug might – by simply shutting down important cytokine production. Cytokines are very much a balance, and they are all important – even the inflammatory ones – so shutting down one or several could lead to some serious problems as a delicate balance is upset. Instead, Maxi Flavone, with its flavonoids and antioxidants, addresses the ROS and inflammation that is causing the release of inflammatory cytokines such as TNF-a.

Finding and correcting the reasons for inflammation such as environmental stresses (air pollution, mold, toxic exposure), subtle or sub-clinical infections (candida, chlamydia, amebiasis), personal stresses (job, sleep, relationships), physical stresses (allergies, food intolerances, hormone imbalances) and nutritional deficiencies or excesses is vital to correcting cytokine imbalances.

The truth is, though we talk a lot about cytokines, there are so many of them and their interactions are so complex that we really don’t have a good understanding of the many interactions and ways that they function. Trying to micro-manage cytokines with individual interventions is probably like throwing cups of water into the ocean to make the level rise.

What we DO know is that cytokines become imbalanced in response to identifiable “macro” insults or imbalances in the body: infections (subtle or obvious), stress (external and internal), toxins — anything that creates an alarm reaction in the body.

Instead of pretending that we understand cytokines and their myriad functions and interactions, a more productive path to health and fertility is to balance the body at the higher levels. The cytokines know how to balance themselves when everything “upstream” in the body is in balance and threats to physical health have been removed.

Support:

Th1 Stimulating Supplements:
Immune-boosting herbs such as echinacea, astragulus, licorice root, ashwaganda, panax ginseng, chlorella, grape seed extract, and common immune-boosting medicinal mushroom extracts, like maitake, reishi, and shitake, will stimulate Th1.

Th2 Stimulating Supplements:

Antioxidants like resveratrol, pycnogenol, curcumin from turmeric, genistein, quercetin, and green tea will stimulate Th2.

Vitamin D is increasingly being recognized for it’s importance in managing healthyTh1/Th2 balance and low vitamin D status is associated with an increased risk of Th1 mediated autoimmune diseases. It has been seen that Vitamin D deficient persons have elevated Th1 cell-associated responses and decreased Th2 cell-associated responses. The antiinflammatory effects of vitamin D are very similar to IL-10 – one o fthe most important antiinflammatory cytokines.

Fish Oil – (EPA / DHA) is highly antiinflammatory. EPA (eicosapentaenoic acid) decreases TNF-a.
EPA and DHA (docosahexaenoic acid) each decrease NK cell activity and this effect is synergistic when both EPA and DHA are used together.

References:

Seydel KB1, Li E, Swanson PE, Stanley SL Jr. Human intestinal epithelial cells produce proinflammatory cytokines in response to infection in a SCID mouse-human intestinal xenograft model of amebiasis. Infect Immun. 1997 May;65(5):1631-9

Mullins BJ1, Kicic A, Ling KM, Mead-Hunter R, Larcombe AN.
Biodiesel exhaust-induced cytotoxicity and proinflammatory mediator production in human airway epithelial cells.Environ Toxicol. 2014 Jul 5

Xiong H1, Wei L, Peng B. IL-17 stimulates the production of the inflammatory chemokines IL-6 and IL-8 in human dental pulp fibroblasts.
Int Endod J. 2014 Jul 5

Sundman E, Olofsson PS. Neural control of the immune system. Adv Physiol Educ. 2014 Jun;38(2):135-9

de Vries MA1, Klop B, Janssen HW, Njo TL, Westerman EM, Castro Cabezas M. Postprandial inflammation: targeting glucose and lipids.
Adv Exp Med Biol. 2014;824:161-70

Ciortea R1, Mihu D, Mihu CM. Association between visceral fat, IL-8 and endometrial cancer. Anticancer Res. 2014 Jan;34(1):379-83

Ali Akoum, Christine Jolicoeur, Abdelaziz Kharfi, and Marie Aubé. Decreased Expression of the Decoy Interleukin-1 Receptor Type II in Human Endometriosis. Am J Pathol. Feb 2001; 158(2): 481–489

Margherita T. Cantorna, Sanhong Yu, and Danny Bruce. The paradoxical effects of vitamin D on Type 1 mediated immunity. Mol Aspects Med. Dec 2008; 29(6): 369–375.Published online May 4, 2008. doi: 10.1016/j.mam.2008.04.004 PMCID: PMC2633636 NIHMSID: NIHMS82537

Matheu V1, Bäck O, Mondoc E, Issazadeh-Navikas S. Dual effects of vitamin D-induced alteration of TH1/TH2 cytokine expression: enhancing IgE production and decreasing airway eosinophilia in murine allergic airway disease.J Allergy Clin Immunol. 2003 Sep;112(3):585-92.

Margherita T Cantorna, Yan Zhu, Monica Froicu, and Anja Wittke. Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system1,2,3,4. 2004 American Society for Clinical Nutrition

Mukaro VR, Costabile M, Murphy KJ, Hii CS, Howe PR, Ferrante A. Leukocyte numbers and function in subjects eating n-3 enriched foods: selective depression of natural killer cell levels. Arthritis Res Ther. 2008;10(3):R57. Epub 2008 May 14.

Ferrucci L, Cherubini A, Bandinelli S, Bartali B, Corsi A, Lauretani F, Martin A, Andres-Lacueva C, Senin U, Guralnik JM. Relationship of plasma polyunsaturated fatty acids to circulating inflammatory markers. J Clin Endocrinol Metab. 2006 Feb;91(2):439-46. Epub 2005 Oct 18.

Sundrarjun T, Komindr S, Archararit N, Dahlan W, Puchaiwatananon O, Angthararak S, Udomsuppayakul U, Chuncharunee S. Effects of n-3 fatty acids on serum interleukin-6, tumour necrosis factor-alpha and soluble tumour necrosis factor receptor p55 in active rheumatoid
arthritis. J Int Med Res. 2004 Sep-Oct;32(5):443-54.

Yamashita N, Sugiyama E, Hamazaki T, Yano S.Inhibition of natural killer cell activity by eicosapentaenoic acid in vivo and in vitro.Biochem Biophys Res Commun. 1988 Jan 15;150(1):497-505.

Yamashita N, Yokoyama A, Hamazaki T, Yano S. Inhibition of natural killer cell activity of human lymphocytes by eicosapentaenoic acid. Biochem Biophys Res Commun. 1986 Aug 14;138(3):1058-67.

Yamashita N, Maruyama M, Yamazaki K, Hamazaki T, Yano S. Effect of eicosapentaenoic and docosahexaenoic acid on natural killer cell activity in human peripheral blood lymphocytes. Clin Immunol Immunopathol. 1991 Jun;59(3):335-45.

Thies F, Nebe-von-Caron G, Powell JR, Yaqoob P, Newsholme EA, Calder PC. Dietary supplementation with eicosapentaenoic acid, but not with other long-chain n-3 or n-6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y. Am J Clin Nutr. 2001 Mar;73(3):539-48.

Cachexia / Catabolism

Natural Support For Unintended Weight Loss

Catabolism means “breaking down” and anabolism means “building up” body tissue. Under normal circumstances, “breaking down” and “building up” are in balance with each other, and a person maintains a consistent weight.

In weight training and weight gain, anabolism or “building up” occurs faster than catabolism, and tissue (fat or muscle) is added to the body. In catabolism, the rate of “breaking down” exceeds the “building up” phase and unintended weight loss results. Cachexia refers to malnutrition and lack of absorption that can cause catabolism.

Causes of cachexia/catabolism include chronic diseases such as tuberculosis and cancer, but catabolism can also occur without the presence of disease. In disease states it is believed that inflammatory substances produced by the body, including interleukin-1 (IL-1), IL-6, interferon gamma and tumor necrosis factor alpha (TNFa) play a role in the progression of cachexia.

Cachexia is a common problem in the elderly. Decreased production of digestive enzymes, plus changes in taste and appetite, often lead to decreased food intake. Total lower calorie consumption results in weight loss.

When the intake of protein falls below critical levels, loss of muscle tissue, including heart muscle, can occur.

When digestion and absorption are decreased, even an adequate amount of calories may not prevent weight loss. Remember, anabolism (“building up”) requires sufficient calories, sufficient protein, and normal digestion and assimilation. The above-listed inflammatory substances may prevent weight gain in spite of adequate caloric nutrition.

Diet And Lifestyle Recommendations

  • Diet MUST include adequate, high quality protein. This is even more important than total calories. High quality protein, especially whey protein, can be added to a “blender drink” to boost protein intake in a highly absorbable form. (See “Dr. Myatt’s Super Shake” recipe).
  • Exercise, especially light weight training, encourages muscle tissue to take up amino acids (protein) from the bloodstream. OVER-exercise is not recommended, but mild to moderate weight training exercise will help build muscle tissue.

Primary Support

  • Maxi Multi: 3 caps, 3 times per day with meals.
  • Protein powder: (alternate between whey and soy or use whey exclusively): 30 grams or more (2 scoops) of protein per day. This can easily (and tastily!) be taken as a “milkshake,” “hot chocolate,” or “pudding.”
  • Similase: 2 caps, 3 times per day with meals. (Digestive enzymes to aid assimilation)
  • L-glutamine: 500-1,000mg, 3 times per day with meals. L-glutamine in powdered form mixes easily with recipes. [Target dose: 3,000-5,000 mg per day].
  • CoQ10 (100mg): 1 cap, 2 times per day with meals.

Additional Support

Dr. Myatt’s Comments (Other Considerations)

A complete physical exam is always in order for unexplained weight loss, since many curable illnesses can cause this problem.

Be sure to have a hormone profile, including thyroid and sex hormones. If you have bowel problems, a Comprehensive Digestive Stool Analysis (CDSA) is in order. Low levels of sex hormones and/or high levels of thyroid or adrenal hormones can cause weight loss. Depending on the results of these tests, your holistic physician may recommend DHEA or other hormones.

How to Calculate Protein & Calorie Requirements

Protein: Multiply your weight by 0.7. This will give you the number of grams of protein you should consume each day. Remember, total protein intake is even more important than total calorie intake, because the body cannot make protein from any other food source (fats or carbohydrates). Protein is necessary for maintenance of muscle mass (including the heart) and for an intact immune system. Excesses of protein can be stored as fat, but excesses of fat, calories, or carbohydrates (starches and sugars) cannot be converted into protein. PROTEIN INTAKE IS OF PRIMARY IMPORTANCE IN CATABOLISM.

Example: 106 pounds (put your body weight here) X 0.7= 74 grams of protein (the amount of protein a 106 pound cachexic person needs each day). Normal or overweight individuals have different protein requirements. Please refer to the “Longevity Protocol” audio tape and paper, page 134 of the Holistic Health Handbook, for precise information on calculating protein and calorie requirements in normal and overweight individuals.

Calories: Multiply your weight in pounds by 18. This will give you the number of calories that you need each day to gain weight. (This number also accounts for a mild to moderate activity level).

Example: 106 pounds (put your body weight here) x 18 = 1908 calories. (Normal or overweight individuals have different calorie requirements. Please refer to the “Longevity Protocol” audio tape and paper for information on calculating protein and calorie requirements in normal and overweight individuals.

REMEMBER: People can survive and be healthy being very lean IF they have sufficient protein to keep muscle mass, heart and the immune system functioning well.

Dr. Myatt’s Final Comment

Non-holistic physicians, upon seeing catabolism in a patient, will often recommend a liquid “milkshake-like” canned “nutritional replacement drink.” These products contain more sugar than protein (you need more protein than sugar) and many artificial additives. They are NOT your “best bet” for restoring body mass. Use your own “Super Shake” with high protein and targeted supplements instead and you can do MUCH better. Whey protein is especially valuable because it contains immune factors and cachexia can cause immune weakness.

Calcium D-Glucarate

Powerful Protection from Environmental Toxins

Calcium D-GlucarateCalcium D-Glucarate, considered to be a longevity booster, is involved in the detoxification of certain xenobiotics, lipid soluble toxins and steroid hormones, and is used for additional support in the Holistic prevention and treatment of breast cancer. Calcium d-glucarate facilitates the excretion of potentially disease-promoting compounds, such as estrogen, and reduces lipid (fat) levels in the blood.

Description- A high-potency natural phytonutrient supplement that supports Phase II glucuronidation pathways.

Suggested dose: 1 – 3 capsules, 3 times daily with meals or as directed.

CANCER


Natural Strategies And Support

Cancer continues to be one fo the most frightening diagnoses that anyone can receive.

Conventional medicine woudl have us believe that there is no possible treatment other than their conventional chemotherapy, radiation, and surgery. No dietary change, no nutritional status improvement, no herb or vitamin, no other treatment can be considered anything but “quackery” and any of those things will be immediately dismissed as useless and even dangerous by most conventional practitioners.

We at the Wellness Club feel differently. We believe that there is no one “magic bullet” to “cure” cancer, and that any approach to cancer must be balanced, rational, and individualized to each person. We believe that in some cases conventional chemotherapy may well be the best treatment. We also believe that conventional treatments, when augmented by natural, holistic treatment, can be made more effective and less toxic.

Leading New Cancer Cases and Deaths – 2013 Estimates

Estimated New Cases*

Estimated Deaths

Male

Female

Male

Female

  1. Prostate
    238,590 (28%)
  2. Lung & bronchus
    118,080 (14%)
  3. Colon & rectum
    73,680 (9%)
  4. Urinary bladder
    54,610 (6%)
  5. Melanoma of the skin
    45,060 (5%)
  6. Kidney & renal pelvis
    40,430 (5%)
  7. Non-Hodgkin lymphoma
    37,600 (4%)
  8. Oral cavity & pharynx
    29,620 (3%)
  9. Leukemia
    27,880 (3%)
  10. Pancreas
    22,740 (3%)

All sites
854,790 (100%)

  1. Breast
    232,340 (29%)
  2. Lung & bronchus
    110,110 (14%)
  3. Colon & rectum
    69,140 (9%)
  4. Uterine corpus
    49,560 (6%)
  5. Thyroid
    45,310 (6%)
  6. Non-Hodgkin lymphoma
    32,140 (4%)
  7. Melanoma of the skin
    31,630 (4%)
  8. Kidney & renal pelvis
    24,720 (3%)
  9. Pancreas
    22,480 (3%)
  10. Ovary
    22,240 (3%)

All sites
805,500 (100%)

  1. Lung & bronchus
    87,260 (28%)
  2. Prostate
    29,720 (10%)
  3. Colon & rectum
    26,300 (9%)
  4. Pancreas
    19,480 (6%)
  5. Liver & intrahepatic bile duct
    14,890 (5%)
  6. Leukemia
    13,660 (4%)
  7. Esophagus
    12,220 (4%)
  8. Urinary bladder
    10,820 (4%)
  9. Non-Hodgkin lymphoma
    10,590 (3%)
  10. Kidney & renal pelvis
    8,780 (3%)

All sites
306,920 (100%)

  1. Lung & bronchus
    72,220 (26%)
  2. Breast
    39,620 (14%)
  3. Colon & rectum
    24,530 (9%)
  4. Pancreas
    18,980 (7%)
  5. Ovary
    14,030 (5%)
  6. Leukemia
    10,060 (4%)
  7. Non-Hodgkin lymphoma
    8,430 (3%)
  8. Uterine corpus
    8,190 (3%)
  9. Liver & intrahepatic bile duct
    6,780 (2%)
  10. Brain & other nervous system
    6,150 (2%)

All sites
273,430 (100%)

 

 

 

 

*Excludes basal and squamous cell skin cancers and in situ carcinoma except urinary bladder.

Data taken from American Cancer Society, Inc., Surveillance Research 2013

Usefull Resources:

Dietary Ketosis In The Treatment of Solid Tissue Malignancy

Prostate Support And PC Spes: A note from Nurse Mark

Botanical and Nutritional Considerations in the Treatment of Prostate Cancer

Prostate Cancer

Breast Cancer Month – And That Little Pink Ribbon Again

Liver Cancer: Is There A One-Pill Treatment?

Cancer Treatment Causes Cancer? Yes!

Cancer Scandal: Poison For Profit

7 Simple Ways to Decrease Your Cancer Risk

Breast Cancer Prevention: Dr. Myatt’s Recommendations

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.
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    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].
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    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.
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    Support Groups

    1.) Gottlieb BH, Wachala ED. Cancer support groups: a critical review of empirical studies. Psychooncology. 2007 May;16(5):379-400.
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    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.
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    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.
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    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
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    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,
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    Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
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    Curr Opin Urol. 2003 Mar;13(2):147-51.
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    Antioxidants (General) and Cancer

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

    1.) Yuan JM, Ross RK, Gao YT, Qu YH, Chu XD, Yu MC. Prediagnostic levels of serum micronutrients in relation to risk of gastric cancer in Shanghai, China. Cancer Epidemiol Biomarkers Prev. 2004 Nov;13(11 Pt 1):1772-80.
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    3.) Kamat AM, Lamm DL. Chemoprevention of bladder cancer. Urol Clin North Am. 2002 Feb;29(1):157-68.
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    Epidemiol Biomarkers Prev. 2002 May;11(5):451-7.
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    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].
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    4.) Bussey HJR, DeCosse JJ, Deschner EE, et al. A randomized trial of ascorbic acid in polyposis coli. Cancer 1982;50:1434–9.
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    Selenium

    1.) Li H, Stampfer MJ, Giovannucci EL, Morris JS, Willett WC, Gaziano JM, Ma J.A prospective study of plasma selenium levels and prostate cancer risk. J Natl Cancer Inst. 2004 May
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    8.) Helzlsouer KJ, Comstock GW, Morris JS. Selenium, lycopene, alpha-tocopherol, ß-carotene, retinol, and subsequent bladder cancer. Cancer Res 1989;49:6144–8.
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    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
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    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.
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    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.
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    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.
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    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.
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    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.
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    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.
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    Grape Seed Extract (Resveratrol)

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    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
    Mar;19(3):419-24.

    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.

Dr. Myatt’s Cardiovascular Risk Checklist

A Medical White Paper Presented By Dr. Dana Myatt

“…As many as fifty percent of all first heart attacks are last heart attacks. Half of all people who have a heart attack die from “sudden cardiac death.” People with NO conventional risk factors are more likely to die “sudden death” from a first heart attack. Sudden cardiac death is the first and only sign of heart disease in this group…”

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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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98.) 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.

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100.) 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.

101.) Hill SM, Spriggs LL, Simon MA, Muraoka H, Blask DE.:The growth inhibitory action of melatonin on human breast cancer cells is linked to the estrogen response system. Cancer Lett. 1992 Jul 10;64(3):249-56.

102.) 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.

103.) Boik, John: Cnacer and Natural Medicine, Oregon Medical Press, 1995,p.71.

104.) Drake EN.: Cancer chemoprevention: Selenium as a prooxidant, not an antioxidant. Med Hypotheses. 2006 Mar 28; [Epub ahead of print]

105.) Zhao R, Xiang N, Domann FE, Zhong W.: Expression of p53 enhances selenite-induced superoxide production and apoptosis in human prostate cancer cells.Cancer Res. 2006 Feb 15;66(4):2296-304.

106.) Sieber F, Daziano JP, Gunther WH, Krieg M, Miyagi K, Sampson RW, Ostrowski MD, Anderson GS, Tsujino I, Bula RJ.: ELEMENTAL SELENIUM GENERATED BY THE PHOTOBLEACHING OF SELENOMEROCYANINE PHOTOSENSITIZERS FORMS CONJUGATES WITH SERUM MACROMOLECULES THAT ARE TOXIC TO TUMOR CELLS.Phosphorus Sulfur Silicon Relat Elem. 2005;180(3-4):647-657.

107.) Wada S, Satomi Y, Murakoshi M, Noguchi N, Yoshikawa T, Nishino H.: Tumor suppressive effects of tocotrienol in vivo and in vitro.Cancer Lett. 2005 Nov 18;229(2):181-91. Epub 2005 Aug 10.

108.) Sylvester PW, Shah SJ, Samant GV.: Intracellular signaling mechanisms mediating the antiproliferative and poptotic effects of gamma-tocotrienol in neoplastic mammary epithelial cells.J Plant Physiol. 2005 Jul;162(7):803-10

109.) Shah SJ, Sylvester PW.: Gamma-tocotrienol inhibits neoplastic mammary epithelial cell proliferation by decreasing Akt and nuclear factor kappaB activity. Exp Biol Med (Maywood). 2005 Apr;230(4):235-41.

Materia Medica References:

1.) Kandil O.M., et al.: Garlic and the immune system in humans: its effect on natural killer cells. Fed Proc 46:441, 1987.

2.) 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.

3.) Lau, B.H., Yamasaki, T., and Gridley, D.S.: Garlic compounds modulate macrophage and T-lymphocyte function. Mol Biother 3:103-107, 1991. 4.) Kandil, O.M. et. al.: Garlic and the immune system in humans: Its effect on natural killer cells. Fed Proc 46:441, 1987.

5.) 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.

6.) Kiesewetter H., et al.: effects of garlic coated tablets in peripheral arterial occlusive disease. Clin Investig 71:383-86, 1993.

7.) Orekhov, A.N., et al.: Direct anti-atherosclerotic related effects of garlic. Ann Med 27:63-65, 1995.

8.) Belman S.: Onion and garlic oils prohibit tumor promotion. Carcinogenesis 4(8):1063-5, 1983.

9.) Dausch JG., Nixon DW.: Garlic: a review of its relationship to malignant disease. Prev Med 19:346-61, 1990.

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11.) Yang, Y.Z., et al.: Effect of Astragalus membranaceus on natural killer cell activity and induction with coxsacke B viral myocarditis. Chin Med J 103:304-7, 1990.

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13.) Chu, D.T., et al.: Immunotherapy with Chinese medicinal herbs, I: Immune restoration of local xenogenic graft-versus-host reaction in cancer patients by fractionated Astragalus membranaceus in vitro. J Clin Lab Immunol 25:119-123, 1988.

15.) Yunde, H., Guoling, M., Shuhua, W., et al.: Effect of radix Astragalus seuhedysari on the interferon system. Chin Med J 94:35-40, 1981.

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18.) Cavallito, C.J., and Bailey, J.H.: Allicin, the antibacterial principal in Allium sativum, I: Isolation, physical properties, and antibacterial action. J Am Chem Soc 66:1950-51,1944.

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.

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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.

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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.

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Dr. Myatt’s Cardiovascular Risk Checklist

A Medical White Paper Presented By Dr. Dana Myatt

February is “Heart Month.” Here’s Your Heart-Risk Checklist.

Shocking Facts about Heart Attacks

February is heart month, and in honor of your heart, I have prepared a special heart-risk assessment and report for you. First, some surprising statistics about heart disease. These “fast facts” will help you know why my heart-risk checklist is so potentially important.

Heart disease is the #1 cause of death in the US.1 2,200 people die every day from heart disease.

As many as 50% of all people who have a heart attack do not have ANY classic risk factors, although one study argues that this number is actually only 20%.  “Only” a 20% chance of having a heart attack with no known risk factors? I don’t know about you, but that still sounds like a big risk to me.

As many as fifty percent (50%) of all first heart attacks are last heart attacks if you get my drift. Half of all people who have a heart attack die from “sudden cardiac death.” No second chances. No “jump-starting” the heart with a defibrillator. No bypass surgery or stents. Just gone in a heartbeat.

People with NO conventional risk factors are more likely to die “sudden death” from a first heart attack.  Sudden cardiac death is the first and only sign of heart disease in this group.

You could be a non-smoker with a normal body weight, total cholesterol below 200, LDL below 100, HDL above 50. You don’t smoke, are not diabetic and have no family history of heart disease. Good for you. You doctor has just given you a clean bill of health and told you your heart is fine. And you could die of a heart attack as you leave the doctor’s office. Remember, twenty to fifty percent of all people who have a heart attack do not have ANY conventionally-tested heart risks.

Emerging Risk Factors: The “Other Risks” No One Is Telling You About

Routinely screened conventional risk factors include blood fats (total cholesterol, LDL, HDL), blood pressure, smoking, and diabetes.4 Additional testing might include a cardiac stress test (the “treadmill test”). Overweight/obesity, family history and activity levels should also be considered.

Unfortunately, 20-50% of people who have heart attacks are “normal” for all of these tests and markers. It’s the folks with “all normal” risk factors who have the greatest likelihood of having a fatal heart attack.

Conventional medicine acknowledges that there are a number of other risk factors for heart disease. These are called “emerging risk factors” because the information is still “emerging” or coming to light.

Unfortunately, tests for these “emerging risk factors” are not yet ordered by most conventional physicians nor are they typically covered by insurance. Many of them will be “standard of care” in conventional medicine some day in the future. Will “some day” be soon enough for you or me?

Good News About “Emerging Risk Factors”

The good news is many of the most important of these “other risks” can be tested at an affordable price. They are not obscure tests with thousand-dollar price tags.

The OTHER good news is that there are safe, natural, proven options for correcting abnormalities if and when they are found. After all, what good would it be to know about a risk factor if there was nothing you could do about it?

To receive your free copy of Dr. Myatt’s Cardiovascular Risk Factors Medical White Paper please enter your name and email address in the area to the right.

Your Medical White Paper will be sent to your email address as a safe and secure .pdf document attachment that can easily be opened by any computer using the free Adobe Reader program.

You will be able to save it to your computer and print it out as needed.

This registration protects us from unauthorized downloading of this important document and protects you from spammers and computer security risks.

Name: Email:

We respect your email privacy

Important: If you have previously downloaded this White Paper (if you are “Already Subscribed”) and you have lost or misplaced your copy please email NurseMark at DrMyattsWellnessClub.com for a replacement.

Please print this Medical White Paper, including the pages of references, so that you can show it to your doctor / cardiologist. When he / she tells you that 1) he has never heard of some of these tests, 2) you don’t need them, 3) he’s not going to order them for you, and 4) your insurance won’t pay for them anyway, please note that Dr. Myatt will make these tests available to you here at a very reasonable cost.

Dr. Myatt’s Cardiovascular Risk Checklist Lab Tests

From Dr. Myatt’s Medical White Paper on Cardiovascular Risk Factors:

“…As many as fifty percent of all first heart attacks are last heart attacks. Half of all people who have a heart attack die from “sudden cardiac death.” People with NO conventional risk factors are more likely to die “sudden death” from a first heart attack. Sudden cardiac death is the first and only sign of heart disease in this group…”

Dr. Myatt has been able to locate and provide a comprehensive Cardiac Risk Profile that includes both currently accepted Cardiac Risk Factors and the New Emerging Cardiac Risk Factors that she discusses in her Medical White Paper.

These “emerging Risk Factors” are the ones that your conventional doctor – even your conventional cardiologist – will not test for.

Sorry – Currently unavailable – please check back soon!

Black Salve Intensive

Resources for Students

Hello Doctors, Herbalists and Interested Others!

Here is part of the promised follow-up resources from our Black Salve Intensive.

Please Note:

  • The information on this page is presented for educational purposes only.
  • This information is based on Dr. Myatt’s clinical experience with Black Salve. It is not intended as “how to” instruction for anyone using Black Salve.
  • As Dr. Myatt explained in her lectures, Black Salve is not recommended for the removal of cancers other than melanoma.
  • Removal of any cancer with Black Salve is “Chemical Surgery.” If you would not be comfortable cutting a lesion out with a scalpel then you should not be considering the use of Black Salve.

Malignant melanoma: practice visual diagnosis

Here are slides of melanoma, but also look at their NON-melanoma pages for comparison.

More practice pictures: comparisons of benign and malignant lesions

Remember, the “big deal” in dermatology is whether or not you can visually be sure of a melanoma. “When in doubt, cut it out (biopsy),” which in the case of melanoma means “cut it out with a big margin” (bummer, since most lesions are NOT melanoma)
OR
apply the black salve for 30 minutes and see if the lesion changes. If it does,
something is abnormal. Take it out. Here is what a suspicious lesion will look
like in 20-30 minutes after application of the black salve: (slide from the Black Salve Intensive will go here as soon as we convert the pic to digital!). Visualize that little white bump you saw in several slides at the conference.

Making Black and Other Salves

Black Salve

The primary ingredients in black salve are blood root (sanguinaria) and zinc chloride, although chaparral and other herbs have also been used.

Black Salve Recipe 1 & 2

Drawing Salve

Remember that drawing salves will contain charcoal and usually also bentonite  clay as the main “magic” in the formula.

Drawing salve #1

Healing Salve

Most healing salves contain some variation on a theme of comfrey, aloe vera, or calendula.

Healing salve with comfrey

Make this with chamomile and comfrey

I will post additional recipes as I find them. If any of you discover a good recipe, please forward it to me for addition to this page.

Buying Black and Other Salves

1.) Best on Earth I haven’t used their black salve but it’s got all the right ingredients and looks like it should work. They also have “after care” salve, AKA “healing salve.” They do NOT carry a drawing salve.

I have used their non-toxic sunscreen and I love it! It’s light, non-greasy, feels wonderful on the skin and doesn’t contain any potentially harmful ingredients. I now use this myself for my daily sunscreen (face and neck).

2.) Sun Spot (glycoalkaloid) cream (for non-melanoma — basal cell and squamous cells, actinic keratosies and other “pre-cancerous” lesions).

Misc. Black Salve Information

Ingredients, pictures and history of black salve. This is a great page with pictures and history of each ingredient.

Bone and Joint Health

Arthritis and Osteoporosis are NOT Inevitable

The bones and joints are often some of the first parts of the body to show signs of aging. Contrary to popular belief, however, the “wear and tear” theory of arthritis has been largely disproved. Although an injury can certainly cause joint damage, most causes of arthritis are not related to “overuse” or injury. We know this because senior marathon runners — who place a lot more “wear and tear” on their joints — actually suffer from less arthritis than non-runners of similar age.

If “wear and tear” isn’t the main causes of joint pain, osteoporosis and arthritis, what is? Decreasing male and female sex hormones, lack of bone nutrients, overweight and obesity, lack of exercise and body-wide inflammation and free-radical damage are some of the most common causes of joint pain and chronic changes such as arthritis. Low gastric acidity, common in people over age 50, impairs the body’s ability to assimilate bone nutrients such as calcium from food and supplements. This should be evaluated with a gastric acid self-test.

Here are some of the top recommendations for maintaining or restoring bone and joint health.

Top Bone and Joint Health Supplements and Herbs

Bone and Joint Therapies
Table of Contents

Bone and Joint
Health Concerns by Topic

Multiple Vitamin/Mineral Formula Arthritis-Osteoarthritis Bromelain Arthritis – Rheumatoid Cal-Mag Amino Back Pain COX2 Low Gastric Acidity Vitamin D Menopause, Female DHEA Menopause, Male (Andropause) Gastric Acid Self-Test Osteoporosis Melatonin Male hormones Female hormones Glucosamine sulfate Grape Seed Extract MSM Strontium Turmeric Other

Multi Vitamin/Mineral Formula – Not a “once per day” pill (they don’t contain enough of anything to have any effect except preventing severe deficiency disease). A complete bone and joint-protecting multiple should include optimal doses (not minimal doses) of B complex vitamins, C, D, K, calcium, magnesium, vanadium, zinc, and boron which are all especially important for strong bones.

If you only take ONE NUTRITIONAL FORMULA for your overall health plus bone and joint health, a quality Optimal Multiple Vitamin/Mineral such as Maxi Multi should be The One.

Bromelain Nature’s Premier Anti-Inflammatory herb,
Bromelain is a mixture of sulfur-containing, protein-digesting enzymes from the stem of Anansus cosmosis (pineapple). Since it was introduced as a medicinal agent in 1957, more than 200 scientific papers on bromelain’s medicinal uses have appeared in the medical literature. It is one of the safest, most well-studied anti-inflammatory herbs known.

Cal-Mag Amino The recommended calcium dose for post-menopausal women or for those with osteoporosis is 1,500 mg calcium with corresponding magnesium, boron and vitamin D. Maxi Multi Daily Multiple formula contains 1000 mg of calcium and 500 mg magnesium per day, which is optimal for most people. Post-menopausal women and anyone with a diagnosis of osteoporosis may need even higher doses. Cal-Mag Amino supplies additional calcium, magnesium, vitamin D and boron is easy-to-assimilate forms.

Cox-2-Support A superior anti-inflammatory herbal formula. Why take dangerous NSAID’s for pain relief when you can take safe this and effective combination?

Vitamin D increases calcium absorption. Deficiencies of Vitamin D are associated with osteoporosis, rheumatic pains, and dental disease. Many authorities are recommending that the RDA should be raised from 400 IU to 1,000 IU. Doses of 1,000-2,000 are not only safe, they may be needed for disease prevention.

DHEA is a steroid hormone secreted by the adrenal glands. It is a precursor (“master hormone”) for many other steroid hormones including male and female sex hormones (estrogen and testosterone) and corticosteroids. DHEA levels often decline dramatically with age.

Low DHEA levels in the brain and blood are thought to contribute to many of the problems associated with aging including age-related memory and mental decline, decreased strength and muscle mass, lowered immune system response, heart disease and atherosclerosis, and age-related weight gain.

Gastric Acid Function Studies have shown that stomach acid production declines with age. Why does this matter? Because a strong stomach acid is necessary to assimilate bone nutrients from food and supplements, including calcium and magnesium (the major bone nutrients). Surprisingly, even symptoms of “excess stomach acid” are usually caused by low, not high, stomach acid. Learn more about gastric acid function here.

Natural Hormone Replacement Therapy (estrogen, progesterone, testosterone, pregnenelone) Both women and men appear to benefit from natural hormone replacement therapy after age 40. By “natural,” I mean using hormones that are identical to what the body manufactures and in amounts that a healthy body produces in early adulthood. This is a very different type of hormone replacement from the semi-synthetic forms and doses used in conventional medicine.

Male hormones: testing and replacement

Female hormones: testing and replacement

Glucosamine Sulfate is the only form of glucosamine proven by over 300 scientific investigations and 20 double-blind studies to stimulate joint repair and relieve pain.

Glucosamine is a molecule manufactured by the body. Inside the joint, it stimulates the production of glycosaminoglycans (GAG’s) which are the main structural material of joints. Studies suggest that a decline of the body’s manufacture of glucosamine may be the primary cause of osteoarthritis.

Grape Seed Extract (OPC’s) is an antioxidant that exhibits 50 times more antioxidant power than vitamin E and 20 times more than vitamin C.

Grape Seed Extract (OPC’s) binds to collagen and helps increase elasticity of skin, muscles, tendons and ligaments. Grape seed extract (OPC’s) has been proven by over 25 years of clinical studies to be useful for stroke prevention (grape seed extract helps keep blood viscosity normal), skin rejuvenation and/or wrinkle prevention (strengthens collagen), arthritis and musculoskeletal complaints (antioxidant and strengthens collagen), blood clot prevention (improves blood viscosity), respiratory allergies (antihistamine), food allergies (antihistamine), asthma (antihistamine), ADHD (many cases are allergy-related), longevity and rejuvenation programs (blood viscosity and collagen-strengthening effects).

MSM (Methylsulfonylmethane)is a source of biologically active sulfur. Sulfur is a mineral that is plentiful in the human body and is found in particularly high concentrations in structural tissues (joints, skin, hair, nails). Unfortunately, sulfur is easily destroyed by cooking. This means that many people have a deficiency of this important joint and skin nutrient.

StrontiumThe “forgotten mineral” that not only prevents, but reverses, osteoporosis. If you are concerned about bone density, this is one mineral you should definitely supplement. Since it competes with calcium and magnesium for absorption, strontium should be taken separately from other bone-building formulas.

TurmericThis bright yellow spice herb is also one of nature’s most potent anti-inflammatory substances. Turmeric (and it’s active ingredient, curcumin), help reduce the pain and swelling of joint inflammation. Turmeric also helps the joints through it’s potent  antioxidant properties.

Other Joint and Bone-Healthy Supplements. Fish and flax oil, Mega Soy, Feverfew, Ginger.

Brain and Memory

Keep a Life-Long Healthy Brain and Memory

There are multiple factors that influence brain and memory health. Simple nutritional deficiencies, heavy metal toxicity, chronic inflammation, vascular disease and even stress are risk factors for memory changes and brain diseases.

Taking steps to prevent or slow memory loss is an important consideration for those people who are using anti-aging and longevity measures. Simple lifestyle, dietary and supplement measures can help ensure clear-thinking and good memory well into old age.

Top Brain and Memory Supplements and Herbs

Brain and Memory Therapies
Table of Contents

Brain and Memory
Health Concerns by Topic

Multiple Vitamin/Mineral Formula Alzheimer’s Disease Acetyl-L-Carnitine Anxiety CoQ10 ADD/ADHD DHEA Dementia (senility) DMAE Depression Essential Fatty Acids (EFA’s) Hypothyroid (Low Thyroid) Gastric Acid Self-Test Memory Loss Ginkgo Neurological Disease (ALS,MS) Ginseng (Panax) Parkinson’s Disease Huperizine Stress Melatonin Male hormones Female hormones Thyroid Vinpocetin

Multiple Vitamin/Mineral Formula. The Standard American Diet (S.A.D.) is typically deficient in essential vitamins, minerals and trace minerals. To compound this problem, older people are at even greater risk for nutrient deficiency because they tend to eat less, although their requirements for certain vitamins, such as B6, actually rise with age. Older people often also have problems with efficient absorption of nutrients from food because of low gastric acid function. Even healthy older people often have deficiencies of vitamin B6, vitamin B12, and folic acid, 3 “B complex” vitamins essential for brain and memory health.

Vitamins and certain minerals are involved in biochemical processes throughout the body and are necessary for protecting cognitive function. The B vitamins are especially important for normal brains and nervous system function and help the brain manufacture chemicals (neurotransmitters) that affect mood.

Filling in the “gaps” in diet with an optimal vitamin/mineral formula such as Maxi Multi is one of the most important steps you can take toward preserving good brain health and sharp memory.

Acetyl-L-Carnitine (ALC), a derivative of the amino acid L-carnitine, is a vitamin-like compound that transports fatty acids (“fuel”) into cells. It has been approved in Europe as a “drug” to treat heart and neurological disease. It also acts as a powerful antioxidant in the brain. The acetyl form of L-carnitine (ALC) was found to be substantially more active than L-carnitine in brain cells.

CoQ10 is a naturally-occurring antioxidant produced in the human body. It is vitally involved in energy production. CoQ10 functions as an “energizer” to mitochondria, the body’s energy producing units. Mitochondria, which produce about 95% of the body’s energy, require CoQ10 to “spark” their production of energy units (ATP). Muscles, and the heart in particular, have high requirements for CoQ10.

CoQ10 is essential to the functioning of the mitochondria and many age-related diseases have been linked to lower mitochondrial function. Since CoQ10 production typically declines by about 50% with age, most longevity specialists consider it one of the most important anti-aging nutrients to supplement.

DHEAis a steroid hormone secreted by the adrenal glands. It is a precursor (“master hormone”) for many other steroid hormones including male and female sex hormones (estrogen and testosterone) and corticosteroids. DHEA levels often decline dramatically with age.

Low DHEA levels in the brain and blood are thought to contribute to many of the problems associated with aging including age-related memory and mental decline, decreased strength and muscle mass, lowered immune system response, heart disease and atherosclerosis, and age-related weight gain.

DMAE (dimethylaminoethanol), found in highest concentrations in anchovies and sardines, is also produced in small amounts in the human brain. DMAE is a precursor to the neurotransmitters choline and acetylcholine, although DMAE crosses the blood-brain barrier faster than choline. Once inside brain cells, DMAE is converted to phosphatidylcholine, a substance used for maintenance and repair of cells, especially brain cells. Studies have shown DMAE to be useful for improved memory and short-term concentration and in
Alzheimer’s dementia.

Essential Fatty Acids(EFA’s). Omega-3 fatty acids, especially docosahexaenoic acid (DHA), has attracted significant attention for its ability to boost brain function. DHA is found in very high concentrations in cell membranes and is required by developing infant brains. Studies have shown that DHA helps protect brain cells by suppressing a neurotoxic substance called amyloid-beta (beta amyloid is a substance found in the brains of Alzheimer’s patients).

Ginkgo is one of the most well-studied herbs for age-related memory changes. It is also a potent antioxidant. Ginkgo increases circulation to small-diameter blood vessels (such as those in the brain and extremities) and inhibits platelet aggregation (decreases blood “stickiness”). Ginkgo also has anti-allergy effects. Ginkgo is one of the best-selling natural remedies worldwide. Many alternative physicians and researchers feel that ginkgo should be part of the Longevity Protocol for everyone over age 50.

Ginseng(Panax spp.) Panax ginseng was considered the “Herb of Emperors” in ancient China, and only the emperor was allowed to use ginseng. This was because the potent effects of ginseng were felt to be “too precious” for the common man.

Modern research has confirmed ginseng’s amazing powers. Ginseng improves immunity through a wide variety of mechanisms. It stimulates DNA synthesis and is useful for anti-aging and chronic disease. Studies have shown that ginseng improves both physical and mental stamina. “It’s not just for the emperor any more!”

Huperizine or Chinese Club moss, contains a substance (Huperizine A) which prevents the breakdown of acetylcholine in the brain. Acetylcholine is a neurotransmitter necessary for memory function. The most promising drugs for Alzheimer’s disease work in the same manner, although Huperizine appears to have a more precise mechanism whereby it protects acetylcholine. Huperizine may be useful for both Alzheimer’s and non-Alzheimer’s memory loss.

Melatonin, a hormone manufactured by the pineal gland, is best-known as an aid for insomnia. Beyond it’s use as a sleep aid, melatonin is also a powerful antioxidant that crosses the blood/brain barrier and helps protect the central nervous system against injury, disease, and aging. Melatonin levels decrease with age, and this reduction in melatonin levels results in many age-related concerns and complaints: sleep difficulties, an increased susceptibility to stress-related diseases, reduced immunity, and increased susceptibility to damage and disease caused by free radicals. Many researchers consider melatonin to be one of the most powerful anti-aging substances available.

Natural Hormone Replacement Therapy (estrogen, progesterone, testosterone, pregnenelone) Both women and men appear to benefit from natural hormone replacement therapy after age 40. By “natural,” I mean using hormones that are identical to what the body manufactures and in amounts that a healthy body produces in early adulthood. This is a very different type of hormone replacement from the semi-synthetic forms and doses used in conventional medicine.

Male hormones: testing and replacement

Female hormones: testing and replacement

Thyroid. Low thyroid function impairs memory and thinking. A test should be performed to determine thyroid function and natural supplements or thyroid replacement therapy should be started if thyroid levels are low.

Vinpocetin is derived from the periwinkle plant. More than 100 studies have shown that vinpocetin increases cerebral circulation (blood supply to the brain) AND improves brain energy production (ATP) and oxygen use. The potential benefits of vinpocetin include treatment of stroke, inner ear problems that result in dizziness, hearing loss, vision loss, neurological disorders, memory loss.