Natural Support Strategies for the most common male cancer in the U.S.

Prostate carcinoma is the most common male cancer in the U.S. It accounts for an estimated 32% of all newly diagnosed cancers. (Other forms of prostate cancer, such as sarcoma, are rare). The incidence of disease increases with each decade of life over age 50. Prostate cancer rates have risen 108% since 1950, believed due in part to earlier detection. Death rates from the disease have increased 23% in spite of widespread use of surgery, radiation and chemotherapy.

There is great debate in the medical community regarding the value of conventional treatment. Prostate cancer is, in most cases, slow-growing. Increased survival rates reported in some studies may be due to earlier detection, not treatment. Many newly diagnosed and early stage cancers in older men would never progress to morbidity or mortality. Considering the risk of impotence (50-60% with surgery), incontinence (from surgery or radiation) and other treatment side-effects, the value of conventional therapy must be questioned in all cases of cancer in older men.

Prostate carcinoma is a hormone-dependent cancer. Therefore, in addition to general immune enhancing and anti-cancer therapies, hormonal manipulation has a role to play in treatment of this disease. Herbal and nutritional treatment for cancer can be considered an adjuvant therapy in all cases of prostate carcinoma and the sole therapy in many cases. Even when conventional treatment is deemed advisable, non-traditional uses of conventional hormone-suppressive drugs (called “Androgen Deprivation Therapy” or ADT), may be safer and more advantageous than standard therapy alone. This is because, in it’s early stages, prostate cancer is highly controllable with hormone-blocking therapy.

Laboratory Evaluation of Prostate Cancer

In additional to generalized immune testing and basic cancer workup (chemistry screen, CBC, TFT’s, etc.), several tests specific to prostate disease allow the clinician to track progression non-invasively and with greater accuracy. These tests include prostatic-specific antigen (PSA), free PSA, prostatic acid phosphatase (PAP), and prolactin.

PSA is now used as the preferred screening test for both benign prostatic hypertrophy (BPH) and prostate cancer. Because PSA may be elevated in both benign and cancerous prostate disease, the test is not specific for prostate cancer. Values in the “indeterminate” range (4-12) present a special diagnostic dilemma. It is further estimated that 25% of men with prostate cancer will have PSA’s less than 4. Taken together, the PSA test poses a significant number of both false-negative and false-positive results. The PSA is an accurate measure of cancer cell activity once the diagnosis has been established.

Free-PSA is a more recent marker that has not yet been universally embraced by conventional medicine. Current research suggests that the free-PSA is a useful “next step” for evaluating elevated PSA’s. In men with PSA’s ranging from 4.1-10, higher levels of free-PSA (18.9 median value) correlated with benign disease while lower levels of free-PSA (10.1 median) correlated with cancer. It is estimated that 95% of “indeterminate” PSA reading could be clarified non-invasively with the additional use of the free-PSA test.

Prostatic acid phosphatase (PAP) was the prostate cancer screening test that preceded use of the PSA. An elevated PAP in a patient with known prostate cancer is indicative of lymphatic spread of the disease.

Prolactin hormone is an additional growth factor to the prostate gland, and rising prolactin levels correlate with progression in advanced prostate cancer cases. Prolactin receptors are found on prostate cancer cells, and it is postulated that these receptors may facilitate the entry of testosterone into the cell. Even with hormone ablation therapy, detectable androgen remains in the blood from adrenal sources. Blocking prolactin secretion may therefore be another method for slowing progression of the disease. It is recommended that prolactin levels be kept below 3 in all patients with hormone-responsive cancers.

Specific Goals of Prostate Cancer Therapy

Testosterone, prolactin, cortisol, insulin, glucose and arachidonic acid-derived prostaglandins (especially PGE2) act as growth factors for prostate cancer. Decreasing circulating levels of these hormones and blocking inflammatory pathways should be undertaken in addition to non-specific cancer therapies such as immune enhancement.


Low saturated fat diets decrease the body’s endogenous and exogenous hormone production. Conversely, diets high in saturated fats decrease NK cell activity and increase arachidonic acid, an inflammatory precursor. Rates of breast, colon, prostate, uterine, ovarian and testicular cancers are significantly higher in countries with high saturated fat intakes. Saturated fats promote inflammatory prostaglandin synthesis while omega-3 fatty acids are anti-inflammatory.

A ketogenic (very low carbohydrate) diet such as The Super Fast Diet decreases the availability of glucose and insulin. Insulin is a growth factor for cancer and the primary metabolic pathway of cancer cells is anaerobic glycolysis, meaning that cancer cells thrive with a high glucose diet. In animal studies, even s slight change toward metabolic acidosis resulted in tumor regression. A low carbohydrate diet which induces ketosis (metabolic acidosis) may duplicate this effect. Overweight patients can afford to lose weight on such a diet, to further reduce their own hormone production. (Fat cells manufacture estrogen, a growth-promoting hormone).

Foods of Special Benefit

Garlic, lemon peel (the peel contains limonene), fish, flax seed, soy and soy products, fresh vegetables (especially non-starchy, dark leafy greens), blueberries and other berries (high in flavonoids and low in sugars), grains (whole grain only, to reduce insulin response and increase fiber content).

Grains should be used sparingly. In patients with more than twenty pounds to lose, they do not need to be used at all until desired weight is achieved.


  • A ketogenic diet such as The Super Fast Diet should be followed to lower insulin and glucose levels.
  • Achieve and maintain an optimal body weight and BMI. (BMI 18-22).
  • Exercise regularly to improve prostate circulation. Walking and running are the best for prostate circulation because they use the major leg muscles. Cycling restricts blood flow to the prostate and testicles and should not be used as the primary form of exercise for men.


  • Maxi Multi: 3 caps, 3 times per day with meals. Optimal (not minimal) doses of vitamin A, carotenes, C, D and selenium appear particularly important.
  • Omega 3 fatty acids:
    Flax seed meal, 2 teaspoons per day with food
    Max EPA (Omega-3 rich fish oil): 1-2 caps, 3 times per day with meals (target dose: 3-6 caps per day). (Or eat fish 3 times per week and use 2 teaspoons of ground flax seed per day added to food).
  • Vitamin D: 1,000-5,000IU per day based on blood test results
  • Bromelain: 1-2 caps, 3-4 times per day between meals.
  • Melatonin: 10-40mg before bed.


(NOTE: These therapies should be undertaken with the guidance of a physician who can order laboratory tests to determine hormone levels and immune function, monitor the effectiveness of treatment, assess possible toxicity and prescribe drugs when advisable). Please strongly consider obtaining a consultation with Dr. Myatt.

To Decrease testosterone

  • Saw palmetto: Serenoa repens, S. serrulata (Palmaceae)
    Saw palmetto blocks the conversion of testosterone to
    dihydrotestosterone (DHT) and there is evidence that DHT may be five times as potent as testosterone in stimulating prostate cancer cell growth.
  • Chaste berry: Vitex agnus-castus, V. negundo (Verbenaceae)-
    Vitex spp. decreases testosterone production in vivo and inhibits prolactin synthesis and release in animal models. As the name “chaste tree” implies, this herb was traditionally used by monks to reduce libido.
  • Rx: Casodex, Flutamide, Lupron, Zoladex

To Decrease prolactin

  • Vitex spp.- Chaste tree
  • Vegetarian diet
  • Rx: Bromocriptine, Pergolide, Dostinex

Vitamin D3 (cholecalciferol): 1,000 I.U., 2-3 times per day with meals.
Vitamin D3 induces prostate cancer cell death (apoptosis) by apparent translocation of the cancer cell androgen receptor. This makes the cell less susceptible to testosterone-induced cell-growth stimulation. D3 encourages cancer cells to become more normal (induces differentiation), inhibits a cancer cell from developing it’s own blood supply (inhibits angiogenesis) and shows antitumor activity. Because vitamin D has the potential to cause toxicity, doses over 1,000 I.U. should be monitored by a physician. Increased blood calcium levels can result from toxicity. In clinical practice, D3 appears to benefit metastatic bone disease in higher doses, perhaps because this vitamin is needed for normal calcification of bone matrix.
Food sources of vitamin D include cold water fish (salmon, mackerel, herring), butter, egg yolks and dark green leafy vegetables. Sunlight acting on the skin will also create vitamin D. In areas of decreased sunlight, increases of breast and colon cancer have been observed.


Prostate cancer, especially early and mid-stage cancers in older patients, respond favorably to natural remedies. Whether as an adjuvant to conventional therapy or as the sole therapy, such treatment strategies should be considered.

Cancer, including prostate cancer, behaves differently depending on the age of the patient, the extent of the disease, the patient’s basic level of health, hormone status, etc., etc. For this reason, cancer patients should seek qualified holistic medical help when designing a natural (adjuvant or primary) treatment protocol.

Digestive enzymes (multi enzymes), whether from animal sources (pancreatin, etc.) or botanical (bromelain, papain), have been shown to increase survival time, inhibit metastasis, and stimulate immune cells. Enzymes induce differentiation and inhibit angiogenesis, possibly through antifibrinolytic mechanisms. It has also been postulated that enzymes may help unmask tumor cells and make them more accessible to the immune system.

Melatonin is a hormone produced by the pituitary gland. It regulates circadian rhythms and plays a role in sleep regulation. It is also a more potent antioxidant than glutathione or vitamin E. In vitro, melatonin demonstrates anti-estrogen activity and immune stimulation. Recent research shows that melatonin inhibits cell proliferation profoundly in vivo but only weakly in vitro. It is synergistic with IL-2 and increases the effectiveness of IL-2 treatment. Dosages used are much higher in cancer treatment than for insomnia or longevity protocols.

Prostate Cancer: Case Studies

The following case studies are meant to highlight for the reader or physician the effects of diet, hormone deprivation therapy, and adjuvant therapy on prostate cancer. Information about new prostate cancer blood tests, as well as new ways to interpret older tests, are also given. Anyone with a diagnosis of cancer should be working with a knowledgeable physician. Cancer can often be controlled through non-invasive measures but regular blood tests are important to verify the success of treatment. The interpretation of such tests is best done in conjunction with a physician. I am available for consultation.

Case # 1:

An otherwise healthy 65 year old male was found on routine physical exam to have a PSA of 19.7. Digital rectal exam (DRE) was unremarkable; Gleason score 2 + 3 on biopsy. Other relevant data: weight 208 pounds, height 5’11″, blood sugar 110, cholesterol 211, triglyceride 244.

The patient had originally declined conventional treatment offered him at the time of diagnosis. He began a self-prescribed regimen of CoQ10, vitamin A,C,E, N-acetyl cystein and MGN3 (mushroom preparation). In four months, his PSA was 14.0, other vitals remained relatively unchanged.

At this point, the patient consulted me. I performed a PAP which was 1.1, normal. I put the patient on a ketogenic diet, substituted Maxi Muli formula for his separate vitamins, added Maxi Greens and vitamin D3. One month later, his PSA was 10.2, weight 189, blood sugar 83, cholesterol 167 and triglycerides 43.

Dr. Myatt’s comments

PSA is an accurate marker of prostate cancer activity after the diagnosis of cancer has been established. Any significant decreases of PSA represent a slowing of the disease process, so this number can be used in early and mid-stage prostate cancer to assess efficacy of treatment. The patient’s initial decrease of PSA was due entirely to his supplement regimen since no diet changes were made at that time.

After beginning The Super Fast Diet, the patient had a further decline in PSA, accompanied by significant improvements in blood sugar, weight, cholesterol, and triglycerides. After two months and four months, the patient’s PSA’s remain at 10.2. A continuing decline is desirable, but this “holding pattern” is still good.

The ketogenic diet made the most dramatic improvement in this case. Not only did it result in further control of the cancer, but the patient is now at lower risk for cardiac and other weight-related problems as well. It is important to remember that a disease such as prostate cancer rarely appears in isolation. Overall improvement of the patient’s health is necessary to gain control of the disease and minimize risk of other diseases. What good is it to save a person from prostate cancer only to have them die of a heart attack?

Case # 2:

An obese (250 pounds+) 56 year old male with a history of asthma was found on routine physical exam to have a PSA of 4.4 and a free PSA of 5.9, suggesting cancer. Biopsy confirmed the diagnosis. During the first four weeks after diagnosis, the patient’s PSA rose from 4.4 to 6.2, a rapid increase suggesting a possibly aggressive cancer. The PAP was within normal limits, indicating no lymphatic or extra-capsular spread.

The patient was advised to follow a The Super Fast Diet (a ketogenic diet), which would be expected to benefit both the cancer and asthma. (Obesity is associated with an increased likelihood of asthma and contributes a large hormone burden to the body because fat cells manufacture estrogen. Estrogen is a growth factor for hormone-related cancers including prostate cancer). The patient has thus far failed to follow a ketogenic diet. Hormone deprivation therapy was initiated, and this dropped the PSA to less the 0.1 in one month, indicating current control of the disease. Since cancer cells eventually “escape” hormone suppression, this treatment will not be expected to work indefinitely. During this time, the patient will be encouraged to lose weight, preferably on a ketogenic diet. I will continue to encourage him to either have surgery or become more dedicated to a non-surgical cancer control program. Prostate cancer is one form of cancer that is highly amenable to diet and lifestyle modification if the individual is willing to make some modest positive changes.

This article is developed from the lecture notes for a lecture presented by Dr. Myatt in May of 2000 at the 2000 Pacific Northwest Herbal Symposium. A transcript of the original, fully annotated notes may be found at the link below:

Botanical and Nutritional Considerations in the
Treatment of Prostate Cancer

Dana Myatt, N.M.D.


Lab Evaluation and Incidence

1.) Beers, Mark M.D., Berkow, Robert M.D. , editors, The Merck Manual of Diagnosis and Therapy, Merck research Laboratories, 1999, p. 1918.
2.) Boik, John, Cancer and Natural Medicine, Oregon Medical Press, 1996, p. 87
3.) Faloon, William, Disease Prevention and Treatment Protocols, Life Extension foundation, Hollywood, FL, 1998, p. 192.
4.) Murphy, Gerald M.D., Lawrence, Walter Jr. M.D., Lenhard, Raymond M.D., Clinical Oncology, American Cancer Society, Atlanta, 1995, p. 315. [copies of this textbook may be obtained by calling your local branch of the American Cancer Society or call 1-800-ACS-2345].
5.) European Journal of Cancer, Vol 31A, No. 6, 1995.

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.

Foods of Special Benefit


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.
3.) Cohen JH, Kristal AR, Stanford JL. Fruit and vegetable intakes and prostate cancer risk. J Natl Cancer Inst 2000;92(1):61–8.
4.) Cohen JH, Kristal AR, Stanford JL. Fruit and vegetable intakes and prostate cancer risk. J Natl Cancer Inst 2000;92(1):61–8.
5.) Kune GA. Eating fish protects against some cancers: epidemiological and experimental evidence for a hypothesis. J Nutr Med 1990;1:139–44 [review].
6.) Rose DP, Connolley JM. Omega-3 fatty acids as cancer chemopreventive agents. Pharmacol Ther 1999;83:217–44.
7.) Demark-Wahnefried W, Price DT, Polascik TJ, et al. Pilot study of dietary fat restriction and flaxseed supplementation in men with prostate cancer before surgery: exploring the effects on hormonal levels, prostate-specific antigen, and histopathologic features. Urology2001;58:47–52.
8.) Davis JN, Singh B, Bhuiyan M, Sarkar FH. Genistein-induced upregulation of p21WAF1, downregulation of cyclin B, and induction of apoptosis in prostate cancer cells. Nutr Cancer 1998;32:123–31.
9.) Barnes S, Peterson TG, Coward L. Rationale for the use of genistein-containing soy matrices in chemoprevention trials for breast and prostate cancer. J Cell Biochem Suppl 1995;22:181–7.
10.) Jacobsen BK, Knutsen SF, Fraser GE. Does high soy milk intake reduce prostate cancer incidence? The Adventist Health Study (United States). Cancer Causes Control 1998;9:553–7.
11.) Geller J, Sionit L, Partido C, et al. Genistein inhibits the growth of human-patient BPH and prostate cancer in histoculture. Prostate 1998;34:75–9.

Body Weight (BMI) and Prostate Cancer

1.) Talamini R, La Vecchia C, Decarli A, et al. Nutrition, social factors and prostatic cancer in a Northern Italian population. Br J Cancer 1986;53:817–21.
2.) Andersson S-O, Wolk A, Bergstrom R, et al. Body size and prostate cancer: a 20-year follow-up study among 135,006 Swedish construction workers. J Natl Cancer Inst 1997;89:385–9.

Exercise and Prostate Cancer

1.) Greenspan SL. Approach to the prostate cancer patient with bone disease. J Clin Endocrinol Metab. 2008 Jan;93(1):2-7.
2.) Barnard RJ, Leung PS, Aronson WJ, Cohen P, Golding LA.A mechanism to explain how regular exercise might reduce the risk for clinical prostate cancer. Eur J Cancer Prev. 2007 Oct;16(5):415-21.
3.) Darlington GA, Kreiger N, Lightfoot N, Purdham J, Sass-Kortsak A. Prostate cancer risk and diet, recreational physical activity and cigarette smoking. Chronic Dis Can. 2007;27(4):145-53.
4.) 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.
5.) Galvão DA, Taaffe DR, Spry N, Newton RU. Exercise can prevent  and even reverse adverse effects of androgen suppression treatment in men with prostate cancer. Prostate Cancer Prostatic Dis. 2007;10(4):340-6. Epub 2007 May 8.
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.) Monga U, Garber SL, Thornby J, Vallbona C, Kerrigan AJ, Monga TN, Zimmermann KP. Exercise prevents fatigue and improves quality of life in prostate cancer patients undergoing radiotherapy. Arch Phys Med Rehabil. 2007 Nov;88(11):1416-22.
8.) 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.

Multiple Vitamins and Cancer / Prostate 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.) Moss RW. Should patients undergoing chemotherapy and radiotherapy be prescribed antioxidants? Integr Cancer Ther. 2006 Mar;5(1):63-82.
4.) 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.
5.) Kristal AR, Stanford JL, Cohen JH, Wicklund K, Patterson RE.Vitamin and mineral supplement use is associated with reduced risk of prostate cancer. Cancer Epidemiol Biomarkers Prev. 1999 Oct;8(10):887-92.

Antioxidants (General) and Prostate Cancer

1.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
3.) Kirsh VA, Hayes RB, Mayne ST, Chatterjee N, Subar AF, Dixon LB, Albanes D, Andriole GL, Urban DA, Peters U; PLCO Trial. Supplemental and dietary vitamin E, beta-carotene, and vitamin C intakes and prostate cancer risk.J Natl Cancer Inst. 2006 Feb 15;98(4):245-54.
4.) Berger MM. Can oxidative damage be treated nutritionally? Clin Nutr. 2005 Apr;24(2):172-83.
5.) Ferguson LR, Philpott M, Karunasinghe N. Dietary cancer and prevention using antimutagens. Toxicology. 2004 May 20;198(1-3):147-59.
6.) Borek C. Dietary antioxidants and human cancer.Integr Cancer Ther. 2004 Dec;3(4):333-41.
7.) Prasad KN. Multiple dietary antioxidants enhance the efficacy of standard and experimental cancer therapies and decrease their toxicity. Integr Cancer Ther. 2004 Dec;3(4):310-22.
8.) Heyland DK, Dhaliwal R, Suchner U, Berger MM. Antioxidant nutrients: a systematic review of trace elements and vitamins in the critically ill patient. Intensive Care Med. 2005 Mar;31(3):327-37. Epub 2004 Dec 17.
9.) Drisko JA, Chapman J, Hunter VJ. The use of antioxidant therapies during chemotherapy. Gynecol Oncol. 2003 Mar;88(3):434-9.
10.) 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.
11.) Lamson DW, Brignall MS. Antioxidants in cancer therapy; their actions and interactions with oncologic therapies. Altern Med Rev. 1999 Oct;4(5):304-29.
12.) 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
13.) 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.
14.) 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 , Carotenes and Prostate Cancer

1.)  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.
2.) 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.
3.) 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.
4.) 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.

Vitamin C and Cancer / Prostate cancer

1.) Hanck A. Vitamin C and cancer. Int J Vit Nutr Res 1983;(Suppl #24):87–104 [review].
2.) 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.
3.)  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.
4.) 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.

Vitamin D and Prostate Cancer

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.)Woo TCS, Choo R, Jamieson M, et al. Pilot study: potential role of vitamin D (cholecalciferol) in patients with PSA relapse after definitive therapy. Nutr Cancer 2005;51:32–6.
5.) 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.
6.) 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.
7.) 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.
8.) 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.
9.) 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.
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.

Selenium and Cancer / Prostate Cancer

1.) Meyer F, Galan P, Douville P, et al. Antioxidant vitamin and mineral supplementation and prostate cancer prevention in the SU.VI.MAX trial. Int J Cancer 2005;116:182–6.
2.) 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.
3.)Clark LC, Combs GF Jr, Turnbull BW, et al. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. JAMA 1996;276:1957–63.
4.)  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.
5.) 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.
6.) Medina D. Mechanisms of selenium inhibition of tumorigenesis. Adv Exp Med Biol 1986;206:465–72.
7.) Willett WC, Polk BF, Morris JS, et al. Prediagnostic serum Selenium and risk of cancer. Lancet 1983;42:130–4.
8.) Beisel WR. Single nutrients and immunity. Am J Clin Nutr 1982;35:417–68.
9.) 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 and Prostate Cancer

1.) Ritch CR, Wan RL, Stephens LB, Taxy JB, Huo D, Gong EM, Zagaja GP, Brendler CB. Dietary fatty acids correlate with prostate cancer biopsy grade and volume in Jamaican men. J Urol. 2007 Jan;177(1):97-101; discussion 101.
2.) Hedelin M, Chang ET, Wiklund F, Bellocco R, Klint A, Adolfsson J, Shahedi K, Xu J, Adami HO, Grönberg H, Bälter KA. Association of frequent consumption of fatty fish with prostate cancer risk is modified by COX-2 polymorphism. Int J Cancer. 2007 Jan 15;120(2):398-405.
3.) Kobayashi N, Barnard RJ, Henning SM, Elashoff D, Reddy ST, Cohen P, Leung P, Hong-Gonzalez J, Freedland SJ, Said J, Gui D, Seeram NP, Popoviciu LM, Bagga D, Heber D, Glaspy JA, Aronson WJ.Effect of altering dietary omega-6/omega-3 fatty acid ratios on prostate cancer membrane composition, cyclooxygenase-2, and prostaglandin E2. Clin Cancer Res. 2006 Aug 1;12(15):4662-70.
4.) Pilot study to explore effects of low-fat, flaxseed-supplemented diet on proliferation of benign prostatic epithelium and prostate-specific antigen. Urology. 2004 May;63(5):900-4.
5.) Augustsson K, Michaud DS, Rimm EB, Leitzmann MF, Stampfer MJ, Willett WC, Giovannucci E. A prospective study of intake of fish and marine fatty acids and prostate cancer. Cancer Epidemiol Biomarkers Prev. 2003 Jan;12(1):64-7.
6.) Dietary fat and cancer.Am J Med. 2002 Dec 30;113 Suppl 9B:63S-70S
7.) Pilot study of dietary fat restriction and flaxseed supplementation in men with prostate cancer before surgery: exploring the effects on hormonal levels, prostate-specific antigen, and histopathologic features. Urology. 2001 Jul;58(1):47-52.
8.) Comparison of fatty acid profiles in the serum of patients with prostate cancer and benign prostatic hyperplasia. Clinical Biochemistry, Vol. 32, August 1999, pp. 405-09.

Bromelain (anasas comosus) and Cancer

1.)Kalra N, Bhui K, Roy P, Srivastava S, George J, Prasad S, Shukla Y.Regulation of p53, nuclear factor kappaB and cyclooxygenase-2 expression by bromelain through targeting mitogen-activated protein kinase pathway in mouse skin.Toxicol Appl Pharmacol. 2008 Jan 1;226(1):30-7. Epub 2007 Aug 23.
2.) Báez R, Lopes MT, Salas CE, Hernández M. In vivo antitumoral activity of stem pineapple (Ananas comosus) bromelain. Planta Med. 2007 Oct;73(13):1377-83. Epub 2007 Sep 24.
3.) Beuth J, Braun JM. Modulation of murine tumor growth and colonization by bromelaine, an extract of the pineapple plant (Ananas comosum L.).In Vivo. 2005 Mar-Apr;19(2):483-5.
4.) Wallace JM. Nutritional and botanical modulation of the inflammatory cascade–eicosanoids, cyclooxygenases, and lipoxygenases–as an adjunct in cancer therapy. Integr Cancer Ther. 2002 Mar;1(1):7-37; discussion 37.
5.) Maurer HR.Bromelain: biochemistry, pharmacology and medical use. Cell Mol Life Sci. 2001 Aug;58(9):1234-45.
6.) Desser L, Holomanova D, Zavadova E, Pavelka K, Mohr T, Herbacek I. Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S10-5.
7.) Hubarieva HO, Kindzel’s’kyĭ LP, Ponomar’ova OV, Udatova TV, Shpil’ova SI, Smolanka II, Korovin SI, Ivankin VS. Systemic enzymotherapy as a method of prophylaxis of postradiation complications in oncological patients] Lik Sprava. 2000 Oct-Dec;(7-8):94-100.
8.) 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.
9.) 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.
10.) 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 and Cancer

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, 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.
6.) 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.

Saw Palmetto (Actions)

1.) Di Silverio F, Monti S, Sciarra A, et al. Effects of long-term treatment with Serenoa repens (Permixon®) on the concentrations and regional distribution of androgens and epidermal growth factor in benign prostatic hyperplasia. Prostate 1998;37:77–83.
2. Strauch G, Perles P, Vergult G, et al. Comparison of finasteride (Proscar®) and Serenoa repens (Permixon®) in the inhibition of 5-alpha reductase in healthy male volunteers. Eur Urol 1994;26:247–52.

Chaste Berry (Vitex) Actions

1.) Sliutz G, Speiser P, Schultz AM, et al. Agnus castus extracts inhibit prolactin secretion of rat pituitary cells. Horm Metab Res 1993;25:253–5.
2.) Böhnert KJ. The use of Vitex agnus castus for hyperprolactinemia. Quart Rev Nat Med 1997;Spring:19–21.