Category: Immune Support

Essential Oils

Concentrated “Plant Hormones”

Essential oils are highly concentrated, volatile oils found in many plants. In plants, they serve a variety of functions similar to human hormones.

Essential oils can be used, diluted, for topical application (all essential oils are highly anti-microbial), aromatherapy, or (in the case of lavender and tea tree) applied directly to the skin (undiluted) for healing.

Lavender Essential Oil – Skin’s Healing Friend

Essential oil of lavender can be applied undiluted to the skin for burns, bites and general irritation. It is the single best healing oil for all skin types. Used as aromatherapy, lavender has a balancing, relaxing and uplifting effect. Apply several drops to a cotton ball or diffuser to help drift peacefully off to sleep.

Myrrh Essential Oil – Soothe Irritated Gums

Essential oil of Myrrh is a classic for healing sore, irritated gums. Apply at gumline with a finger or Q-tip swab.

Myrrh Essential Oil is increasingly expensive and difficult to obtain. Dr. Myatt is able to special-order this rare oil but availability, price, and delivery times are variable. Please call for a quote.

Tea Tree Essential Oil – Nature’s Anti-Fungal

Essential Oil of Tea Tree can be applied directly to the skin for fungal infections, including toe and fingernail fungus, athlete’s foot, jock itch and ringworm.

ESSENTIAL FATTY ACIDS (EFA)

An Explanation Of These “Must-Have” Nutrients

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

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

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

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

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

Glossary of Fats

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

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

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

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

Echinacea (E. angustifolia, purpura)

Natural Immune System Booster

Echinacea - Purple ConeflowerEchinacea is one of the most popular herbs for stimulating and boosting the immune system. It acts as an immune stimulant, immune modulator (balances the immune system), anti-viral and anti-bacterial.

Echinacea, also known as the purple coneflower, is a native American herb with an impressive record of laboratory and clinical research. Echinacea has long been used by North American Plains Indians shamans and today thousands of modern healers use echinacea for treating infectious diseases.  It was often used in modern American medicine in the early 20th Century, and became popular with Europeans, who have used it extensively since the 1930s. Today millions of Europeans use echinacea as a primary therapy for colds, flu’s, infections, and for it’s general immune-boosting effects.

Primary uses of echinacea include:

  • Colds, coughs and flu and other upper respiratory conditions
  • Enlarged lymph glands, sore throat
  • Urinary tract infections
  • Other minor infections
  • May help combat herpes and candida
  • Wounds, skin regeneration and skin infections (external use)
  • Psoriasis, eczema and inflammatory skin conditions (external use)

Echinacea increases the “non-specific” activity of the immune system stimulating the overall activity of the cells responsible for fighting all kinds of infection. Unlike antibiotics, which are directly toxic to bacteria, echinacea makes our own immune cells more efficient in attacking bacteria, viruses and abnormal cells, including cancer cells.

Echinacea facilitates wound healing and reduces the symptoms of and speeds recovery from viral infections. It’s anti-inflammatory effects make it useful externally against inflammatory skin conditions including psoriasis and eczema. It may also increase resistance to candida, bronchitis, herpes, and other infectious conditions.

Hundreds of scientific studies have documented the chemistry, pharmacology, and clinical applications of echinacea. The most consistently proven effect of echinacea is in stimulating phagocytosis, which is to encourage white blood cells and lymphocytes to attack invading organisms.

Specific actions of echinacea include:

  • increases the number and activity of immune system cells, including anti-tumor cells:
  • promotes T-cell activation;
  • stimulates new tissue growth for wound healing;
  • reduces inflammation in arthritis and inflammatory skin conditions;
  • Mild antibiotic action: bacteriostatic, anti-viral, anti-fungal.
  • inhibits the bacterial enzyme hyaluronidase, to help prevent bacterial access to healthy cells.

Specific studies of echinacea include:

  • An extract of echinacea showed an increase of 50%-120% in immune function over a 5 day period (Jurcic, et al. 1989).
  • An extract of echinacea significantly increased the resistance to flu and reduced the symptoms of lymph gland swelling, inflamed nasal passages and headache (Braunig, et al. 1992).
  • Of 4500 patients with inflammatory skin conditions, including psoriasis, 85% were cured with topical applications of echinacea salve (Wacker & Hilbig, 1978).
  • Human white blood cells, stimulated by echinacea extract increased phagocytosis (consumption) of yeast cells by 20-40% compared to controls. (Wagner and Proksch 1985)

Echinacea has an excellent safety record and there is no known toxicity. However, according to the German Kommission E, echinacea should not be used in progressive systemic and auto-immune disorders such as tuberculosis, leicosis, connective tissue disorders, collagenosis and related diseases such as lupus. Further, its use in AIDS or opportunistic infections in AIDS patients is controversial.

It should be noted that echinacea is not appropriate for chronic use: with such long-term use, echinacea appears to lose it’s effectiveness. Maximum periods of continuous use should not exceed 6 – 8 weeks.

Echinacea is not a substitute for other medical interventions in rapidly accelerating infections. If a condition persists or worsens, seek medical advice. Many serious medical conditions are not appropriate for self-diagnosis or self-medication and require the supervision of qualified health care providers.

Additional Reading and References:

  • Echinacea, Nature’s Immune Enhancer by Stephen Foster. Healing Arts Press, 1991.
  • Echinacea, the Immune Herb by Christopher Hobbs. Botanica Press, 1990.
  • Botanical Influences on Illness by Melvyn Werbach and Michael Murray. Third Line Press, 1994. See chapters on Cancer, Candidiasis, Immunodepression, Infection, Wound Healing.
  • Herbal Medicine by Rudolf Weiss. AB Arcanum, 1988.
  • The Lancet Infectious Diseases 2007; 7:473-480 Review Evaluation of echinacea for the prevention and treatment of the common cold: a meta-analysis http://www.thelancet.com/journals/laninf/article/PIIS1473309907701603/abstract
  • British Herbal Pharmacopeia, 1992.
  • Kommission E Monographs: Echinacea. Kooperation Phytopharmaka, , Germany.
  • Jurcic, et al. Zeitschrift fur Phytotherapie 10 (2), 1989.
  • Braunig, et al. Zeitschrift fur Phytotherapie 13: 7-13, 1992.
  • Wagner and Proksch 1985 In: Economic and Medicinal Plant Research, Academic Press, Orlando, p.113.
  • Wacker & Hilbig. Planta Medica 33(1): 89-102, 1978.
  • Chone & Mandakis. Deutsch Med. Wschr. 27: p. 1406
  • Luettig, et al. J. Natl. Cancer Inst. 81(9): 669-75, 1989.
  • Stimpel, et al. Infect. Immun. 46, 845, 1984;
  • Steinmuller, et al. Int. J. Immunopharmac., Vol. 15, No. 5, pp. 605-614, 1993.

Eczema


An Itchy Childhood Problem

Eczema, while it may seem similar to psoriasis, is actually quite different. It is also a disease that can leave a parent feeling helpless and frantic to find relief for their child.

Fortunately, eczema tends to be a disease of childhood – most kids outgrow this itchy problem. Unfortunately, they can be miserable until they do outgrow it.

There is little agreement in conventional medicine about causes and treatments for eczema beyond those offered by the drug companies – that is, antibiotics, corticosteroids, and antihistamines – all of which have undesirable side effects.

So, what can be done? Is there some natural substance or herb that will relieve the itch and help clear up the problem quickly?

Sadly, no. Eczema is a complicated condition, and there is not a simple solution.

Since there are so many things that can cause or contribute to the problem, there are a number of things that should be looked at when seeking relief. I’ll do my best to offer some places for a parent to start.

Allergies: Perhaps the first place to look is at diet – for dietary allergies and eczema seem to go together frequently. Food allergy testing can be very helpful, and a good-old-fashioned elimination / challenge diet can be revealing. Either form of food allergy testing – the high-tech blood-test or the elimination / challenge diet – will offer best results when interpreted with the assistance of a knowledgeable doctor. For little people, the elimination / challenge diet testing may be less distressing and challenging, though more time consuming, than the blood test. More information about food allergies can be found here.

Other allergies can trigger eczema symptoms as well. Pet dander, dust mites – anything which can trigger an allergic reaction – all should be carefully sought out and exposures reduced or eliminated if possible.

Sugar – Many scientists and dermatological researchers feel there is a strong connection between sugar intake and eczema symptoms. Many parents report that a sugar-free diet goes a long way toward lessening their child’s suffering. Sugar is well known to compromise immune function for several hours after ingestion, and sugar intake can contribute to both candida and bacterial overgrowths. For kids this means that fruit juices, sweetened cereals, sugary jams and jellies, syrups, and other sweet treats are a definite no-no. Moms, do your kids a favor and read the labels on foods: Cut out the high-fructose corn syrup, evaporated cane juice, natural cane sugar, or whatever other misnomer the Big Food Corporations use to disguise dextrose / sucralose / fructose / lactose – sugar. Your kids may complain at first that they are being deprived of their sugary junk, but if you persevere you will be rewarded with a big improvement in overall health and behavior as well as with reduced eczema symptoms.

Drugs and Alternatives: Conventional doctors will suggest antihistamine drugs – Benadryl is one popular suggestion – but these can be sedating and have other undesirable side effects. Grape Seed Extract is a far more natural choice with excellent antihistamine properties and no known side effects – it is well worth a try.

Often, after children have been prescribed a round or two of antibiotics (and what child hasn’t had antibiotics!) the normal intestinal flora (the good gut bugs that help us to digest and assimilate our foods) can be seriously compromised. A good probiotic like Suprema-Dophylus can help to restore this balance.

Bathing can dry the skin – and especially during the winter when kids are indoors (and not getting as dirty while playing) daily bathing may not be necessary. Brief baths (what we nurses call “top and tail”) using minimal soap may be all that’s needed. Brisk rubbing and scrubbing of irritated areas is definitely not what you should be doing –  try a brief gentle wash, using warm water not hot, mild unscented soaps,  gentle drying (blotting dry, not rubbing) and mild unscented moisturizers applied to the whole body to help keep that nice moist skin from drying out. Some parents have reported good results using zinc-oxide based creams such as diaper rash creams applied to irritated areas to promote healing. Just remember, as always, unscented is best!

Humidity – or more precisely a lack of humidity as can occur during the winter heating season – can be problematic. A whole-house humidifier can have whole-family benefits, but if that is not possible then a small humidifier wherever the child spends the most can be helpful. Even simple pans of water on or near heating sources can help increase humidity and provide relief.

Temperature – Many parents report that an overly-warm child is an itchy child – especially at night. A slightly cooler sleeping area, and not being heavily bundled may be helpful to reduce nighttime itching. Wool can be itchy even to those not sensitive to it – as can some synthetics. Cotton is often the best for children’s pajamas, and loose-fitting PJs can be more irritating than the snug-fitting knit variety.

Clothing and bedding should be washed in unscented detergents, and double-rinsed to ensure that no soaps remain to cause irritation. Dryer sheets and other softeners should be avoided since they impart potentially irritating scents and chemical residues to clothes.

Fingernails must be kept short and edges and corners rounded to prevent damage when the child scratches – and babies and children will scratch no matter how often you tell them not to! Clean mittens or socks to cover a baby’s hands can be helpful – but children may not be so tolerant and may be less likely to keep them on for long.

When scratching does happen, cool compresses to itchy areas can be soothing – this is nothing more complicated than just a washcloth soaked in cool water and wrung out and held to the area.

Finally, many parents report that stress plays a part in triggering or exacerbating symptoms – too busy a schedule, too many activities, stress at school or with homework – remember, kids need someone to talk to about stress. Also remember that your stress rubs off on your children! Try not to nag at them about scratching at the rashes and try to not be too stressed about the rashes themselves.

Eczema in kids can be a challenge – but with patience and perseverance almost every case can be improved.

 

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.

Consultations With Dr. Dana Myatt

Help Yourself To Good Health

Notice To New Patients:

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

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

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

DANA MYATT, N.M.D.

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

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

 

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DR. DANA MYATT
Help Yourself to Health

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Do Doctors Still Make House Calls?

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

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

Your Own Private Naturopathic Doctor And Nurse – In Attendance:

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

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

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

Is your situation more urgent?

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

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

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

Piper Warrior II Private Airplane
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Brief Consultations

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

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

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

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

Medical records and other documentation can be sent to:

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

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

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:

Coleus Forskohlii (Forskolin)

Enzyme and Hormone Activator

Coleus Forskohlii, a member of the mint family, has a long history of use in Ayurvedic medicine, being applied to a variety of conditions including hypertension, asthma, eczema, psoriasis, congestive heart failure, and angina. The beneficial effects of this herb have been well-researched in both animal and human clinical studies. It acts by increasing levels of cyclic adenosine monophosphate (cAMP) in cells. This cAMP activates many other enzymes which are involved in diverse cell functions. Some of the effects that have been observed and studied include:

A powerful anti-spasmodic action on smooth muscle. This makes it useful for the relief of intestinal colic, uterine cramps, painful (cramping) urination, angina and hypertension. This antispasmodic effect also relaxes airways, resulting in bronchodilation, decreased airway resistance, and increased vital capacity and forced expiratory volume of the lungs, making it a very useful treatment for asthma and allergies.

Increased contractility of the heart muscle, which makes it valuable in the treatment of congestive heart failure, while at the same time it lowers blood pressure by relaxing the arteries.

Increased cerebral (brain) blood flow. This indicates that it may be helpful in improving post-stroke recovery.

Inhibition of platelet aggregation (blood clotting) also adds to its value in the treatment of cardiovascular and cerebrovascular disorders.

It is felt that the cAMP elevating effects of forskolin may result in an improvement in glaucoma and conditions of  increased intraocular pressure.

Symptoms of psoriasis have been improved through the use of forskolin, thought to be due to an improvement in the cAMP/cGMP ratio.

Depression may also be responsive to the effects of forskolin through it’s action of increasing cAMP and inhibiting phosphodiesterase. Researchers stopped short of recommending forskolin for the treatment of depression, but did state that “elevated brain cAMP levels are closely linked to antidepressant activity…”

Scientists at the Penn State University College of Medicine found significant weight loss and reduction of blood pressure levels in subjects of a recent study, indicating that forskolin may be a useful and safe herb for those seeking to lose weight.

Related to the above is the effect that forskolin has on the thyroid: it serves to increase thyroid hormone production and stimulates thyroid hormone release. This mechanism may be one way in which forskolin promotes a normal body weight. It’s effects in normalizing thyroid function may also contribute the antidepressant effects seen with forskolin use.

Scientists at Brown University have suggested that forskolin may have a place in the prevention of tumor metastasis due to its effect as a potent inhibitor of platelet aggregation and inhibition of tumor colonization.

Finally, forskolin has been shown to enhance and boost the immune system by activating macrophages and lymphocytes which are valuable tools in the body’s battle against infection.

Suggested dose: 1-3 capsules per day. (Target: 10-30 mg forskolin per day)

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.

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.
    6.) Kandil O.M., et al.: Garlic and the immune system in humans: its effect on natural killer cells. Fed Proc 46:441, 1987.
    7.) Kandil, O.M. et. al.: Garlic and the immune system in humans: Its effect on natural killer cells. Fed Proc 46:441, 1987.
    8.) Belman S.: Onion and garlic oils prohibit tumor promotion. Carcinogenesis 4(8):1063-5, 1983.
    9.) Kroning, F.: Garlic as an inhibitor for spontaneous tumors in predisposed mice. Acta Unio Inter Contra Cancrum 20(3):855, 1964.

    Super Foods

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

    Exercise and Cancer

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

    Support Groups

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

    Stop Tobacco and Alcohol Use

    1.) Kaufman EL, Jacobson JS, Hershman DL, Desai M, Neugut AI. Effect of breast cancer radiotherapy and cigarette smoking on risk of second primary lung cancer. J Clin Oncol. 2008 Jan 20;26(3):392-8.
    2.) Park SM, Lim MK, Jung KW, Shin SA, Yoo KY, Yun YH, Huh BY. Prediagnosis smoking, obesity, insulin resistance, and second primary cancer risk in male cancer survivors: National Health Insurance Corporation Study. J Clin Oncol. 2007 Oct 20;25(30):4835-43.
    3.) Koskinen WJ, Brøndbo K, Mellin Dahlstrand H, Luostarinen T, Hakulinen T, Leivo I, Molijn A, Quint WG, Røysland T, Munck-Wikland E, Mäkitie AA, Pyykkö I, Dillner J, Vaheri A,
    Aaltonen LM. Alcohol, smoking and human papillomavirus in laryngeal carcinoma: a Nordic prospective multicenter study. J Cancer Res Clin Oncol. 2007 Sep;133(9):673-8. Epub 2007 May 8.
    4.) Muwonge R, Ramadas K, Sankila R, Thara S, Thomas G, Vinoda J, Sankaranarayanan R. Role of tobacco smoking, chewing and alcohol drinking in the risk of oral cancer in Trivandrum, India: A nested case-control design using incident cancer cases. Oral Oncol. 2007 Oct 12
    5.) Chen CH, Shun CT, Huang KH, Huang CY, Tsai YC, Yu HJ, Pu YS. Stopping smoking might reduce tumour recurrence in nonmuscle-invasive bladder cancer. BJU Int. 2007 Aug;100(2):281-6; discussion 286. Epub 2007 Apr 5.
    6.) Rieck G, Fiander A.The effect of lifestyle factors on gynaecological cancer. Best Pract Res Clin Obstet Gynaecol. 2006 Apr;20(2):227-51.
    7.) Ford MB, Sigurdson AJ, Petrulis ES, Ng CS, Kemp B, Cooksley C, McNeese M, Selwyn BJ, Spitz MR, Bondy ML.Effects of smoking and radiotherapy on lung carcinoma in breast carcinoma
    survivors. Cancer. 2003 Oct 1;98(7):1457-64.
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    15;73(6):1541-3.
    10.) Day GL, Blot WJ, Shore RE, McLaughlin JK, Austin DF, Greenberg RS, Liff JM, Preston-Martin S, Sarkar S, Schoenberg JB, et al. Second cancers following oral and pharyngeal cancers: role of tobacco and alcohol. J Natl Cancer Inst. 1994 Jan 19;86(2):131-7.
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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
    cancer: an exploratory study. Adv Mind Body Med. 2000 Fall;16(4):276-87.
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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,
    part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
    2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival,
    Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
    3.) Tsao SM, Yin MC, Liu WH. Oxidant stress and B vitamins status in patients with non-small cell lung cancer. Nutr Cancer. 2007;59(1):8-13.
    4.) Moss RW. Should patients undergoing chemotherapy and radiotherapy be prescribed antioxidants? Integr Cancer Ther. 2006 Mar;5(1):63-82.
    5.) Moyad MA. The use of complementary/preventive medicine to prevent prostate cancer recurrence/progression following definitive therapy. Part II–rapid review of dietary supplements.
    Curr Opin Urol. 2003 Mar;13(2):147-51.
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    7.) Kamat AM, Lamm DL. Diet and nutrition in urologic cancer. W V Med J. 2000 May-Jun;96(3):449-54.
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    10.) Jatoi A, Daly BD, Kramer G, Mason JB. A cross-sectional study of vitamin intake in postoperative non-small cell lung cancer patients. J Surg Oncol 1998;68:231–6.
    11.) Lamm DL, Riggs DR, Shriver JS, vanGilder PF, Rach JF, DeHaven JI. Megadose vitamins in bladder cancer: a double-blind clinical trial. J Urol. 1994 Jan;151(1):21-6.

    Antioxidants (General) and Cancer

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

    Vitamin A and Carotenes

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

    Vitamin C

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

    Selenium

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

    Omega 3 Essential Fatty Acids

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

    CoQ10

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

    Vitamin C – high dose or IV

    1.) Yeom CH, Jung GC, Song KJ. Changes of terminal cancer patients’ health-related quality of life after high dose vitamin C administration. J Korean Med Sci. 2007 Feb;22(1):7-11.
    2.) Shoichiro Ohtani, Arifumi Iwamaru, Wuguo Deng, Kentaro Ueda, Guanglin Wu, Gitanjali Jayachandran, Seiji Kondo, Edward N. Atkinson, John D. Minna, Jack A. Roth and Lin Ji. Tumor Suppressor 101F6 and Ascorbate Synergistically and Selectively Inhibit Non–Small Cell Lung Cancer Growth by Caspase-Independent Apoptosis and Autophagy. Cancer Research 67, 6293-6303, July 1, 2007.
    3.) Sebastian J. Padayatty, Hugh D. Riordan, Stephen M. Hewitt, Arie Katz, L. John Hoffer and Mark Levine. Intravenously administered vitamin C as cancer therapy: three cases. CMAJ
    2006;174(7):937-42.
    4.) Riordan HD, Casciari JJ, González MJ, Riordan NH, Miranda-Massari JR, Taylor P, Jackson JA.A pilot clinical study of continuous intravenous ascorbate in terminal cancer patients. PR
    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
    17.) Menon LG, Kuttan R, Kuttan G. Anti-metastatic activity of curcumin and catechin. Cancer Lett 1999;141:159–65.
    18.) Khafif A, Schantz SP, Chou TC, Edelstein D, Sacks PG. uantitation of chemopreventive synergism between (-)-epigallocatechin-3-gallate and curcumin in normal, premalignant
    and malignant human oral epithelial cells. Carcinogenesis. 1998
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    Vitamin D

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

    Bromelain (anasas comosus)

    1.)Kalra N, Bhui K, Roy P, Srivastava S, George J, Prasad S, Shukla Y.Regulation of p53, nuclear factor kappaB and cyclooxygenase-2 expression by bromelain through targeting mitogen-activated protein kinase pathway in mouse skin.Toxicol Appl Pharmacol. 2008 Jan
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    2002 Mar;1(1):7-37; discussion 37.
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    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
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    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.