Category: Health Concerns

Children’s Basic Nutrients

Kids Need Great Supplements Too!

Thorne Children's Basic NutrientsOptimal nutrition is even more important for children because growing bodies depend on vitamins and minerals normal development. Children soak up nutrients like sponges! However, the majority of children’s multiple vitamin-mineral supplements contain sugar and/or cheap, poorly-absorbed nutrients, tablet binders, and excipients. Children’s Basic Nutrients contains the finest, most bioavailable nutrients, in a small, easy-to-swallow, kid-size capsule. The two-part gelatin capsule may also be taken apart and the contents emptied into food or liquid. This formula is for children age four and older.

Dosage: 1 to 2 capsules three times daily.

Six Small Capsules Contain:
Vitamin B12…. 135.0mcg
Folate…. 240.0mcg
Pantothenic Acid…. 124.0mg
Calcium…. 90.0mg
Iron…. 4.5mg
Iodine…. 67.5mg
Vitamin B6…. 3.0mg
Magnesium…. 85.0mg
Vitamin D…. 120.0I.U.
Zinc…. 4.5mg
Selenium…. 60.0mcg
Copper…. 0.45mg
Manganese…. 1.8mg
Chromium…. 60.0mcg
Molybdenum…. 30.0mcg
Thiamine…. 12.0mg
Vitamin A…. 4500.0I.U.
Vitamin E…. 120.0I.U.
Riboflavin…. 3.3mg
Potassium…. 27.0mg
Boron…. 0.9mg
Choline Citrate…. 30.0mg
Vanadium…. 30.0mcg
Vitamin B3…. 49.0mg
Vitamin C…. 250.0mg
Vitamin K…. 30.0mcg
Biotin…. 120.0mcg

Chlorophyll (water soluble)

For Intestinal Detoxification

Chlorophyll is a water-soluble substance derived from plants. It acts as a natural detoxifier.

We no longer carry pure chlorophyll (Inner Fresh Pro) but instead recommend Maxi Greens or Greens First as a way to obtain full-spectrum chlorophyll and other plant phytonutrients.

HIGH CHOLESTEROL

Natural Treatment And Support Strategies

High cholesterol levels (above 200mg/dl) are associated with an increased risk of atherosclerosis, and atherosclerosis is a leading cause of heart disease, strokes, and other circulatory disorders. Fortunately, since most cases of high cholesterol are caused by diet and lifestyle, they can be reversed by self-care measures. If cholesterol levels do not improve in 12 weeks of self-care, consult an holistic physician for further guidance.

It is also important to note that cardiovascular disease can occur in people with normal cholesterol levels. In fact, half of the people who have a heart attack have a cholesterol level under 200. Total cholesterol levels are important, but they are far from being the entire story of what causes atherosclerosis and heart disease. Other risk factors, such as elevated homocysteine and CReactive Protein (hs-CRP), are independent risk factors. To truly determine your risk for heart disease, consult a holistic physician who can evaluate each of your risk factors, not just cholesterol. Many people with cholesterol levels below 200 mg/dl still suffer heart attacks and stroke.

DIET AND LIFESTYLE RECOMMENDATIONS

  • Maintain a normal body weight.
  • Eat “Super Foods,” especially garlic and soy products. Fiber in food and/or supplements helps bind cholesterol and carry it out of the body. Be sure your diet is high in fiber.
  • Engage in regular aerobic exercise.
  • Do not smoke.
  • Drink 64 ounces of pure water daily. Water detoxifies the liver, which is the organ responsible for managing cholesterol in the body.

PRIMARY SUPPORT

  • Maxi Multi: 3 caps, 3 times per day with meals. This daily “multiple” contains high potency antioxidants. Optimal (not minimal) doses of antioxidants (ACES), calcium, magnesium, selenium, chromium, bioflavonoids and B complex vitamins are particularly important for normal cholesterol levels.
  • 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 (50-100mg): 1 cap, 2-3 times per day with meals (target dose range: 150-400mg per day).
  • Flush-Free Niacin: Begin with 1 cap, 3 times per day with meals. After two weeks, increase dose to 2 caps, 3 times per day or as directed by a physician (target dose range: 1,500-3,000mg per day). Liver enzymes should be monitored by a physician every 3 months for the first six months of treatment. [NOTE: In the Coronary Drug Project Study, niacin was compared to cholesterol-lowering drugs. It was found that niacin was the ONLY “drug” that lowered mortality. It compared favorably to cholesterol-lowering drugs in effect but with a much better safety profile.]
    AND/OR
  • Red Rice Yeast (600mg): 2 caps, 2 times per day with meals (target dose: minimum 2,000mg per day).

Take Red Rice Yeast in addition to niacin if 8 weeks of niacin therapy does not lower cholesterol to <220mg/dl cholesterol. Take instead of niacin if niacin is not well tolerated.

ADDITIONAL SUPPORT

  • Oral ChelatoRx: 4 capsules, 2 times per day between meals. This formula contains garlic, gugulipid, EDTA (chelating agent), chlorella, magnesium, potassium, and more. It is a comprehensive formula for lowering cholesterol levels and clearing the arteries.
  • Garlic (Garlitrin): 1 tab per day (target dose: minimum 4,000 allicin per day).

TESTS

  • Thyroid function tests should be performed to rule out low thyroid function. These are conventional medical tests that most medical doctors will order as part of a physical. (It should be included in a physical work-up for high cholesterol). Conventional doctors usually only do a TSH test for screening, but T3 and T4 should also be evaluated.

Dr. MYATT’S COMMENTS

  • If you are overweight, a ketogenic diet, particularly The Super Fast Diet, will help you easily lose weight, lower your cholesterol and blood pressure, and correct high blood sugar levels if they exist.
  • There are so many natural treatments for high cholesterol, and cholesterol-lowering drugs have so many negative side effects, that it is worthwhile to work with an holistic physician if your self-help measures fail to improve cholesterol levels in three to six months.
  • Be SURE to supplement CoQ10 if you are taking cholesterol-lowering drugs (statins) or Red Rice Yeast, as these drugs deplete CoQ10. Adequate CoQ10 levels are necessary for normal heart function.

CHRONIC FATIGUE SYNDROME (CFS/CVFS)

Natural Support Strategies For This Debilitating Condition

There are many causes of chronic fatigue. Low thyroid function, low adrenal gland function, anemia, diabetes, food allergies, chronic candida infection, blood pressure abnormalities, and low blood sugar are just a few of the many possibilities. For this reason, it is important to consult a physician for diagnosis.

One cause of chronic fatigue is associated with several known viruses. Chronic fatigue of viral origin is now known as Chronic Viral Fatigue Syndrome (CVFS). Symptoms include recurrent sore throats, low grade fever, headache, lymph node enlargement, muscle and joint aches, intestinal discomfort, mood disorder and lack of concentration. The following recommendations apply to chronic fatigue of viral origin:

DIET AND LIFESTYLE RECOMMENDATIONS

  • Do not smoke. Smoking suppresses the immune system.
  • Avoid simple sugars, alcohol, caffeine and food allergens. Eat “Super Foods” plentifully, especially garlic.
  • Exercise. Moderate exercise stimulates immune function.
  • Practice stress reduction techniques. Excess stress response lowers immune function and makes a person more susceptible to viral infection.

PRIMARY SUPPORT

  • Maxi Multi: 3 caps, 3 times per day with meals. This daily “multiple” contains high potency antioxidants. Optimal (not minimal) doses of vitamin A, beta carotene, vitamin C, zinc, selenium, magnesium & B complex vitamins are particularly important.
  • Dr. Myatt’s Immune Boost: 1/2 – 1 tsp., 2-3 times per day between meals.
    AND/OR
  • Immune Support: 2 caps, 2-3 times per day between meals.
  • Co Q10 (50mg): 1 capsule, 2-3 times per day with meals. (Target dose: 100-200mg per day).
  • St. John’s Wort (Hypericum) (300mg): 1 cap, 3 times per day between meals. (Target dose: 900mg per day) Although best know for it’s mood effects, hypericum is also a potent anti-viral agent.

ADDITIONAL SUPPORT (Use any or all of the following)

Digestion, liver, large intestine (colon), and immune system are likely imbalanced organ systems that should be looked at. Be sure to take the “Lifestyle” questionnaire, found on page 2 of the Holistic Health Handbook. Imbalances in diet and insufficient exercise contribute to lowered immune function.

DR. MYATT’S COMMENTS
It is important to consult a physician for diagnosis of chronic fatigue. Do NOT assume that your fatigue is due to a virus until other causes have been eliminated. These “other causes” include thyroid imbalance, sex hormone imbalance, nutritional deficiency, blood sugar problems (too high or too low), blood pressure abnormalities, emotional stress, over or under exercise, or lack of sleep to name just a few.

CLA (Conjugated Linoleic Acid)

The Fat that Makes You Thin

CLA (Conjugated Linoleic Acid) is a naturally-occurring component in beef and milk. CLA has been shown to decrease body fat while increasing lean muscle tissue. Hence, it is useful for both weight loss and weight gain (muscle gaining) programs. Studies also show that CLA improves immunity and helps prevent atherosclerosis and breast cancer.

From Medscape

“May 28, 2004 — Conjugated linoleic acid (CLA) supplementation reduced body fat mass (BFM) in healthy, overweight adults, according to the results of a randomized, double-blind trial published in the June issue of the American Journal of Clinical Nutrition.”

Dr. Myatt’s comment: Use CLA for both weight loss and weight gain diets to preserve and increase lean muscle mass.

Suggested dose:
4-5 caps (1,000mg) per day. (Target dose: 4,000 to 5,000 mg per day)

COLDS AND FLU

Natural Support For These Common Afflictions

Colds and flu are caused by one of over a hundred different strains of viruses. Vaccinations for cold and flu are sometimes useful in people with weak immune systems, but vaccinations alone do not offer complete protection due to the many strains of viruses that cause colds and flu.
Symptoms of common cold include nasal discharge with sneezing and sore throat, usually without fever. Flu is characterized by fever, cough, headache, malaise and cold symptoms.

DIET AND LIFESTYLE

  • Have light broths and soups only during acute phase. Avoid fruit juice and all sugars (Sugar suppresses the immune system).
  • Drink 64 ounces of pure water or herb teas daily, more if fever is present.
  • Bed rest is important.

PRIMARY SUPPORT

ADDITIONAL SUPPORT

For nasal congestion:

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

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    Selenium

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    14.) Beisel WR. Single nutrients and immunity. Am J Clin Nutr 1982;35:417–68.
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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
    Oct;21(10):1010-7.
    10.) Schley PD, Jijon HB, Robinson LE, Field CJ. Mechanisms of omega-3 fatty acid-induced growth inhibition in MDA-MB-231 human breast cancer cells. Breast Cancer Res Treat. 2005
    July;92(2):187-95.
    11.) de Deckere EA. Possible beneficial effect of fish and fish n-3 polyunsaturated fatty acids in breast and colorectal cancer. Eur J Cancer Prev. 1999 Jul;8(3):213-21.
    12.) Chang WL, Chapkin RS, Lupton JR. Fish oil blocks azoxymethane-induced rat colon tumorigenesis by increasing cell differentiation and apoptosis rather than decreasing cell
    proliferation. J Nutr. 1998 Mar;128(3):491-7.
    13.) Bagga D, Capone S, Wang HJ, Heber D, Lill M, Chap L, Glaspy JA. Dietary modulation of omega-3/omega-6 polyunsaturated fatty acid ratios in patients with breast cancer. J Natl Cancer Inst. 1997 Aug 6;89(15):1123-31.

    CoQ10

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

    Vitamin C – high dose or IV

    1.) Yeom CH, Jung GC, Song KJ. Changes of terminal cancer patients’ health-related quality of life after high dose vitamin C administration. J Korean Med Sci. 2007 Feb;22(1):7-11.
    2.) Shoichiro Ohtani, Arifumi Iwamaru, Wuguo Deng, Kentaro Ueda, Guanglin Wu, Gitanjali Jayachandran, Seiji Kondo, Edward N. Atkinson, John D. Minna, Jack A. Roth and Lin Ji. Tumor Suppressor 101F6 and Ascorbate Synergistically and Selectively Inhibit Non–Small Cell Lung Cancer Growth by Caspase-Independent Apoptosis and Autophagy. Cancer Research 67, 6293-6303, July 1, 2007.
    3.) Sebastian J. Padayatty, Hugh D. Riordan, Stephen M. Hewitt, Arie Katz, L. John Hoffer and Mark Levine. Intravenously administered vitamin C as cancer therapy: three cases. CMAJ
    2006;174(7):937-42.
    4.) Riordan HD, Casciari JJ, González MJ, Riordan NH, Miranda-Massari JR, Taylor P, Jackson JA.A pilot clinical study of continuous intravenous ascorbate in terminal cancer patients. PR
    Health Sci J. 2005 Dec;24(4):269-76.

    Grape Seed Extract (Resveratrol)

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

    Turmeric (Curcumin)

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

    1.) Lappe J, Travers-Gustafson D, Davies K, Recker R, Heaney R. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. American Journal of Clinical Nutrition. Am J Clin Nutr. 2007 Jun;85(6):1586-91.
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    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.
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    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.
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    Lycopene

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    Larch arabinogalactin

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    Modified Citrus Pectin

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    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
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    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.