CANCER

Natural Strategies And Support

What if you’ve already been diagnosed with cancer? The first thing to remember is — don’t panic. Cancer is not a death sentence. Many good treatments for cancer exist. A few are found in conventional medicine. Many others are available in natural, alternative and “unconventional” medicine. Non-toxic treatments for cancer have been used successfully by many people, with and without conventional treatment.

If you are going to use alternative treatments, OR if you decide to integrate natural and alternative treatments with conventional care, it is best to seek the help of a qualified “integrative” practitioner. (Someone like myself who uses all avenues of medicine, from conventional to natural, with the foremost regard for the patient’s welfare — not the type of treatment used).

The type of cancer, it’s location, the age and health of the patient, all make a difference as to what the best course of action will be. For example, juice fasting has helped some people but should be strictly avoided by others. Certain medications and surgeries are helpful in some types of cancer, useless in others.

All of these questions need to be answered with the assistance of an holistic physician who can help you determine the best course of action to take and will work with you to sort out the legitimate treatments from the “hype.” There is no room for guesswork and inexperience once a diagnosis of cancer has been made. (Please, consider obtaining a consultation with Dr. Myatt).

DIET AND LIFESTYLE RECOMMENDATIONS

  • Eat a low carbohydrate diet with as much organically-produced food as possible. (The primary “fuel” of cancer cells is glucose, or sugar).  Include plenty of “Super Foods,” especially fresh garlic. Do NOT juice fast or undergo other radical diets until you have conferred with an holistic physician.
  • Drink 64 ounces of pure water daily.
  • Exercise moderately if you are able. Walking is one of the best. Your holistic physician can work with you to design an optimal exercise program.
  • Attend a support group. Studies have shown that people fare better with cancer when they attend such support groups.
  • Stop negative health habits immediately! This includes smoking or other tobacco use and alcohol.
  • Practice meditation, relaxation, prayer or your chosen form of spiritually-directed activity.

PRIMARY SUPPORT

      • Maxi Multi: 3 caps, 3 times per day with meals. Optimal (not minimal) doses of antioxidants (ACES), are particularly important. Many nutrients help prevent side effects from chemotherapy and radiation, but be sure to check with your holistic physician to insure that there are no unwanted interactions with various chemotherapy medications.
      • Omega 3 fatty acids:
        Flax seed meal, 2 teaspoons per day with food
        OR
        Flax seed capsules
        : 2-4 caps, 3 times per day (target dose range: 6-12 caps per day)
        OR
        Flax seed oil
        : 1 tablespoon per day
        OR
        Max EPA
        (Omega-3 rich fish oil): 1-2 caps, 3 times per day with meals (target dose: 3-6 caps per day).
      • CoQ10: 50-300mg per day. This powerful antioxidant, produced by the body, diminishes with age. It is especially valuable for all types of heart disease. CHOLESTEROL-LOWERING DRUGS deplete CoQ10.
      • Vitamin C: take an additional 3,000-10,000mg per day in divided doses. Some studies show that IV vitamin C may be more effective.
      • Turmeric: 1-2 caps, 3 times per day with meals
      • Vitamin D: 1,000-5,000IU per day based on blood test results
      • Bromelain: 1-2 caps, 3 times per day between meals
      • Melatonin: 3-20mg at bedtime (DO NOT use in lymphoma or melanoma)ADDITIONAL SUPPORT

        For Breast Cancer

         

      • Calcium D-glucarate: 2-3 caps, 3 times per day with meals or as directed.
      • Diindolymethane (DIM): 2 caps, 2 times per day.
        For Prostate Cancer

         

      • Lycopene: (15mg): 1 capsule per day with a meal.

 

For all cancers (anti-metastatic)

Note: If you have been diagnosed with cancer and want to explore your options, it is most important to seek qualified help. DO NOT rely on second-hand stories from well-meaning friends and family members. Good treatments, and combinations of treatments, exist for many types of cancers, but relying on anecdotal stories and unproven “remedies” can be a waste of time and money. More importantly, unproven treatments can lead you away from legitimately helpful treatments.

 

Dr. Myatt is available for consultations by telephone. She does extensive research and teaching in the field of both conventional cancer treatment and alternative therapies.


References

Low Carbohydrate Diet

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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

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

Support Groups

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

Stop Tobacco and Alcohol Use

1.) Kaufman EL, Jacobson JS, Hershman DL, Desai M, Neugut AI. Effect of breast cancer radiotherapy and cigarette smoking on risk of second primary lung cancer. J Clin Oncol. 2008 Jan 20;26(3):392-8.
2.) Park SM, Lim MK, Jung KW, Shin SA, Yoo KY, Yun YH, Huh BY. Prediagnosis smoking, obesity, insulin resistance, and second primary cancer risk in male cancer survivors: National Health Insurance Corporation Study. J Clin Oncol. 2007 Oct 20;25(30):4835-43.
3.) Koskinen WJ, Brøndbo K, Mellin Dahlstrand H, Luostarinen T, Hakulinen T, Leivo I, Molijn A, Quint WG, Røysland T, Munck-Wikland E, Mäkitie AA, Pyykkö I, Dillner J, Vaheri A,
Aaltonen LM. Alcohol, smoking and human papillomavirus in laryngeal carcinoma: a Nordic prospective multicenter study. J Cancer Res Clin Oncol. 2007 Sep;133(9):673-8. Epub 2007 May 8.
4.) Muwonge R, Ramadas K, Sankila R, Thara S, Thomas G, Vinoda J, Sankaranarayanan R. Role of tobacco smoking, chewing and alcohol drinking in the risk of oral cancer in Trivandrum, India: A nested case-control design using incident cancer cases. Oral Oncol. 2007 Oct 12
5.) Chen CH, Shun CT, Huang KH, Huang CY, Tsai YC, Yu HJ, Pu YS. Stopping smoking might reduce tumour recurrence in nonmuscle-invasive bladder cancer. BJU Int. 2007 Aug;100(2):281-6; discussion 286. Epub 2007 Apr 5.
6.) Rieck G, Fiander A.The effect of lifestyle factors on gynaecological cancer. Best Pract Res Clin Obstet Gynaecol. 2006 Apr;20(2):227-51.
7.) Ford MB, Sigurdson AJ, Petrulis ES, Ng CS, Kemp B, Cooksley C, McNeese M, Selwyn BJ, Spitz MR, Bondy ML.Effects of smoking and radiotherapy on lung carcinoma in breast carcinoma
survivors. Cancer. 2003 Oct 1;98(7):1457-64.
8.) van Leeuwen FE, Klokman WJ, Stovall M, Hagenbeek A, van den Belt-Dusebout AW, Noyon R, Boice JD Jr, Burgers JM, Somers R. Roles of radiotherapy and smoking in lung cancer following Hodgkin’s disease. J Natl Cancer Inst. 1995 Oct 18;87(20):1530-7.
9.) Neugut AI, Murray T, Santos J, Amols H, Hayes MK, Flannery JT, Robinson E. Increased risk of lung cancer after breast cancer radiation therapy in cigarette smokers. Cancer. 1994 Mar
15;73(6):1541-3.
10.) Day GL, Blot WJ, Shore RE, McLaughlin JK, Austin DF, Greenberg RS, Liff JM, Preston-Martin S, Sarkar S, Schoenberg JB, et al. Second cancers following oral and pharyngeal cancers: role of tobacco and alcohol. J Natl Cancer Inst. 1994 Jan 19;86(2):131-7.
11.) Day GL, Shore RE, Blot WJ, McLaughlin JK, Austin DF, Greenberg RS, Liff JM, Preston-Martin S, Sarkar S, Schoenberg JB, et al. Dietary factors and second primary cancers: a follow-up of oral and pharyngeal cancer patients. Nutr Cancer. 1994;21(3):223-32.

Meditation, Relaxation, Prayer

1.) Cunningham AJ, Phillips C, Lockwood GA, Hedley DW, Edmonds CV. Association of involvement in psychological self-regulation with longer survival in patients with metastatic
cancer: an exploratory study. Adv Mind Body Med. 2000 Fall;16(4):276-87.
2.) Greer S. Improving quality of life: adjuvant psychological therapy for patients with cancer. Support Care Cancer. 1995 Jul;3(4):248-51.

Multiple Vitamins and Cancer

1.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival,
part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival,
Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
3.) Tsao SM, Yin MC, Liu WH. Oxidant stress and B vitamins status in patients with non-small cell lung cancer. Nutr Cancer. 2007;59(1):8-13.
4.) Moss RW. Should patients undergoing chemotherapy and radiotherapy be prescribed antioxidants? Integr Cancer Ther. 2006 Mar;5(1):63-82.
5.) Moyad MA. The use of complementary/preventive medicine to prevent prostate cancer recurrence/progression following definitive therapy. Part II–rapid review of dietary supplements.
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6.) Moyad MA. Potential lifestyle and dietary supplement options for the prevention and postdiagnosis of bladder cancer. Urol Clin North Am. 2002 Feb;29(1):31-48, viii.
7.) Kamat AM, Lamm DL. Diet and nutrition in urologic cancer. W V Med J. 2000 May-Jun;96(3):449-54.
9.) Jatoi A, Daly BD, Kramer G, Mason JB. A cross-sectional study of vitamin intake in postoperative non-small cell lung cancer patients. J Surg Oncol 1998;68:231–6.
10.) Jatoi A, Daly BD, Kramer G, Mason JB. A cross-sectional study of vitamin intake in postoperative non-small cell lung cancer patients. J Surg Oncol 1998;68:231–6.
11.) Lamm DL, Riggs DR, Shriver JS, vanGilder PF, Rach JF, DeHaven JI. Megadose vitamins in bladder cancer: a double-blind clinical trial. J Urol. 1994 Jan;151(1):21-6.

Antioxidants (General) and Cancer

1.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
2.) Simone CB 2nd, Simone NL, Simone V, Simone CB. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
3.) Kirsh VA, Hayes RB, Mayne ST, Chatterjee N, Subar AF, Dixon LB, Albanes D, Andriole GL, Urban DA, Peters U; PLCO Trial. Supplemental and dietary vitamin E, beta-carotene, and vitamin C intakes and prostate cancer risk.J Natl Cancer Inst. 2006 Feb 15;98(4):245-54.
4.) Berger MM. Can oxidative damage be treated nutritionally? Clin Nutr. 2005 Apr;24(2):172-83.
5.) Ferguson LR, Philpott M, Karunasinghe N. Dietary cancer and prevention using antimutagens. Toxicology. 2004 May 20;198(1-3):147-59.
6.) Borek C. Dietary antioxidants and human cancer.Integr Cancer Ther. 2004 Dec;3(4):333-41.
7.) Prasad KN. Multiple dietary antioxidants enhance the efficacy of standard and experimental cancer therapies and decrease their toxicity. Integr Cancer Ther. 2004 Dec;3(4):310-22.
8.) Heyland DK, Dhaliwal R, Suchner U, Berger MM. Antioxidant nutrients: a systematic review of trace elements and vitamins in the critically ill patient. Intensive Care Med. 2005 Mar;31(3):327-37. Epub 2004 Dec 17.
9.) Kim YT, Kim JW, Choi JS, Kim SH, Choi EK, Cho NH. Relation between deranged antioxidant system and cervical neoplasia. Int J Gynecol Cancer. 2004 Sep-Oct;14(5):889-95.
10.) Drisko JA, Chapman J, Hunter VJ. The use of antioxidant therapies during chemotherapy. Gynecol Oncol. 2003 Mar;88(3):434-9.
11.) Prasad KN, Cole WC, Kumar B, Prasad KC. Scientific rationale for using high-dose multiple micronutrients as an adjunct to standard and experimental cancer therapies. J Am Coll Nutr. 2001 Oct;20(5Suppl):450S-463S; discussion 473S-475S.
12.) Lamson DW, Brignall MS. Antioxidants in cancer therapy; their actions and interactions with oncologic therapies. Altern Med Rev. 1999 Oct;4(5):304-29.
13.) Prasad KN, Kumar A, Kochupillai V, Cole WC. High doses of multiple antioxidant vitamins: essential ingredients in improving the efficacy of standard cancer therapy. J Am Coll Nutr. 1999
Feb;18(1):13-25.
14.) Lupulescu A. The role of vitamins A, beta-carotene, E and C in cancer cell biology. Int J Vitam Nutr Res. 1994;64(1):3-14.
15.) Stähelin HB. Critical reappraisal of vitamins and trace minerals in nutritional support of cancer patients. Support Care Cancer. 1993 Nov;1(6):295-7.

Vitamin A and Carotenes

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

Vitamin C

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

Selenium

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

Omega 3 Essential Fatty Acids

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

CoQ10

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

Vitamin C – high dose or IV

1.) Yeom CH, Jung GC, Song KJ. Changes of terminal cancer patients’ health-related quality of life after high dose vitamin C administration. J Korean Med Sci. 2007 Feb;22(1):7-11.
2.) Shoichiro Ohtani, Arifumi Iwamaru, Wuguo Deng, Kentaro Ueda, Guanglin Wu, Gitanjali Jayachandran, Seiji Kondo, Edward N. Atkinson, John D. Minna, Jack A. Roth and Lin Ji. Tumor Suppressor 101F6 and Ascorbate Synergistically and Selectively Inhibit Non–Small Cell Lung Cancer Growth by Caspase-Independent Apoptosis and Autophagy. Cancer Research 67, 6293-6303, July 1, 2007.
3.) Sebastian J. Padayatty, Hugh D. Riordan, Stephen M. Hewitt, Arie Katz, L. John Hoffer and Mark Levine. Intravenously administered vitamin C as cancer therapy: three cases. CMAJ
2006;174(7):937-42.
4.) Riordan HD, Casciari JJ, González MJ, Riordan NH, Miranda-Massari JR, Taylor P, Jackson JA.A pilot clinical study of continuous intravenous ascorbate in terminal cancer patients. PR
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
Mar;19(3):419-24.

Vitamin D

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

Bromelain (anasas comosus)

1.)Kalra N, Bhui K, Roy P, Srivastava S, George J, Prasad S, Shukla Y.Regulation of p53, nuclear factor kappaB and cyclooxygenase-2 expression by bromelain through targeting mitogen-activated protein kinase pathway in mouse skin.Toxicol Appl Pharmacol. 2008 Jan
1;226(1):30-7. Epub 2007 Aug 23.
2.) Báez R, Lopes MT, Salas CE, Hernández M. In vivo antitumoral activity of stem pineapple (Ananas comosus) bromelain. Planta Med. 2007 Oct;73(13):1377-83. Epub 2007 Sep 24.
3.) Beuth J, Braun JM. Modulation of murine tumor growth and colonization by bromelaine, an extract of the pineapple plant (Ananas comosum L.).In Vivo. 2005 Mar-Apr;19(2):483-5.
4.) Wallace JM. Nutritional and botanical modulation of the inflammatory cascade–eicosanoids, cyclooxygenases, and lipoxygenases–as an adjunct in cancer therapy. Integr Cancer Ther.
2002 Mar;1(1):7-37; discussion 37.
5.) Maurer HR.Bromelain: biochemistry, pharmacology and medical use. Cell Mol Life Sci. 2001 Aug;58(9):1234-45.
6.) Desser L, Holomanova D, Zavadova E, Pavelka K, Mohr T, Herbacek I. Oral therapy with proteolytic enzymes decreases excessive TGF-beta levels in human blood. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S10-5.
7.) Beuth J, Ost B, Pakdaman A, Rethfeldt E, Bock PR, Hanisch J, Schneider B. Impact of complementary oral enzyme application on the postoperative treatment results of breast cancer patients–results of an epidemiological multicentre retrolective cohort study. Cancer
Chemother Pharmacol. 2001 Jul;47 Suppl:S45-54.
8.) Tysnes BB, Maurer HR, Porwol T, Probst B, Bjerkvig R, Hoover F. Bromelain reversibly inhibits invasive properties of glioma cells.Neoplasia. 2001 Nov-Dec;3(6):469-79.
9.) Dale PS, Tamhankar CP, George D, Daftary GV. Co-medication with hydrolytic enzymes in radiation therapy of uterine cervix: evidence of the reduction of acute side effects. Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S29-34.
10.) Hubarieva HO, Kindzel’s’kyĭ LP, Ponomar’ova OV, Udatova TV, Shpil’ova SI, Smolanka II, Korovin SI, Ivankin VS. Systemic enzymotherapy as a method of prophylaxis of postradiation
complications in oncological patients] Lik Sprava. 2000 Oct-Dec;(7-8):94-100.
11.) Eckert K, Grabowska E, Stange R, Schneider U, Eschmann K, Maurer HR. Effects of oral bromelain administration on the impaired immunocytotoxicity of mononuclear cells from mammary tumor patients. Oncol Rep. 1999 Nov-Dec;6(6):1191-9.
12.) Zavadova E, Desser L, Mohr T. Stimulation of reactive oxygen species production and cytotoxicity in human neutrophils in vitro and after oral administration of a polyenzyme preparation. Cancer Biother. 1995 Summer;10(2):147-52.
13.) Taussig SJ, Batkin S. Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharmacol. 1988 Feb-Mar;22(2):191-203.
14.) Batkin S, Taussig SJ, Szekerezes J. Antimetastatic effect of bromelain with or without its proteolytic and anticoagulant activity. J Cancer Res Clin Oncol. 1988;114(5):507-8.

Melatonin

1.) Lissoni P, Barni S, Mandalà, et al. Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal hormone melatonin in metastatic solid tumour patients with poor clinical status. Eur J Cancer 1999;35:1688–92.
2.) Lissoni P, Cazzanga M, Tancini G, et al. Reversal of clinical resistance to LHRH analogue in metastatic prostate cancer by the pineal hormone melatonin: efficacy of LHRH analogue plus melatonin in patients progressing on LHRH analogue alone. Eur Urol 1997;31:178–81.
3.) Lissoni P, Paolorossi F, Tancini G, et al. Is there a role for melatonin in the treatment of neoplastic cachexia? Eur J Cancer 1996;32A:1340–3.
4.) Lissoni P, Paolorossi F, Tancini G, et al. A phase II study of tamoxifen plus melatonin in metastatic solid tumour patients. Br J Cancer 1996;74:1466–8.
5.) Lissoni P, Brivio O, Brivio F, et al. Adjuvant therapy with the pineal hormone melatonin in patients with lymph node relapse due to malignant melanoma. J Pineal Res 1996;21:239–42.
6.) Lissoni P, Barmo S. Meregalli S, et al. Modulation of cancer endocrine therapy by melatonin: a phase II study of tamoxifen plus melatonin in metastatic breast cancer patients progressing under tamoxifen alone. Br J Cancer 1995;71:854–6.
7.) Reiter RJ, Melchiorri D, Sewerynek E, Poeggeler B, Barlow-Walden L, Chuang J, Ortiz GG, Acuna-Castroviejo D.: A review of the evidence supporting melatonin’s role as an antioxidant.J
Pineal Res. 1995 Jan;18(1):1-11.
8.) Neri B, Fiorelli C, Moroni F, et al. Modulation of human lymphoblastoid interferon activity by melatonin in metastatic renal cell carcinoma. Cancer 1994;73:315–9.
9.) Lissoni P, Barni S, Cazzaniga M, Ardizzoia A, Rovelli F, Brivio F, Tancini G.: Efficacy of the concomitant administration of the pineal hormone melatonin in cancer immunotherapy with low-dose IL-2 in patients with advanced solid tumors who had progressed on IL-2 alone. Oncology. 1994 Jul-Aug;51(4):344-7.
10.) Lissoni P, Barni S, Ardizzoia A, et al. A randomized study with the pineal hormone melatonin versus supportive care alone in patients with brain metastases due to solid neoplasms. Cancer 1994;73:699–701.
11.) Lissoni P, Barni S, Tancini G, et al. A randomised study with subcutaneous low-dose interleukin 2 alone vs interleukin 2 plus the pineal neurohormone melatonin in advanced solid neoplasms other than renal cancer and melanoma. Br J Cancer 1994;69:196–9.
12.) Aldeghi R, Lissoni P, Barni S, et al. Low-dose interlekin-2 subcutaneous immunotherapy in association with the pineal hormone melatonin as a first-line therapy in locally advanced or metastatic hepatocellular carcinoma. Eur J Cancer 1994;30A:167–70.
13.) Lissoni P, Brivio F, Ardizzoia A, et al. Subcutaneous therapy with low-dose interlekin-2 plus the neurohormone melatonin in metastatic gastric cancer patients with low performance status.
Tumori 1993;79:401–4.
14.) Lissoni P, Barni S, Ardizzoia A, et al. Randomized study with the pineal hormone melatonin versus supportive care alone in advanced nonsmall cell lung cancer resistant to a first-line
chemotherapy containing cisplatin. Oncology 1992;49:336–9.
15.) Lissoni P, Barni S, Crispino S, et al. Endocrine and immune effects of melatonin therapy in metastatic cancer patients. Eur J Cancer Clin Oncol 1989;25:789–95.

Calcium D-glucarate

1.) Singh J, Gupta KP. Induction of apoptosis by calcium D-glucarate in 7,12-dimethyl benz [a] anthracene-exposed mouse skin. J Environ Pathol Toxicol Oncol. 2007;26(1):63-73.
2.) Hanausek M, Walaszek Z, Slaga TJ. Detoxifying cancer causing agents to prevent cancer. Integr Cancer Ther. 2003 Jun;2(2):139-44.
3.) Calcium-D-glucarate. Altern Med Rev. 2002 Aug;7(4):336-9.[No authors listed].
4.) Walaszek Z, Szemraj J, Narog M, Adams AK, Kilgore J, Sherman U, Hanausek M. Metabolism, uptake, and excretion of a D-glucaric acid salt and its potential use in cancer prevention. Cancer Detect Prev. 1997;21(2):178-90.
5.) Heerdt AS, Young CW, Borgen PI. Calcium glucarate as a chemopreventive agent in breast cancer. Isr J Med Sci. 1995 Feb-Mar;31(2-3):101-5.

Di-indolymethanes (DIM, IC3)

1.) Moiseeva EP, Almeida GM, Jones GD, Manson MM.Extended treatment with physiologic concentrations of dietary phytochemicals results in altered gene expression, reduced growth, and apoptosis of cancer cells. Mol Cancer Ther. 2007 Nov;6(11):3071-9.
2.) Weng JR, Tsai CH, Kulp SK, Wang D, Lin CH, Yang HC, Ma Y, Sargeant A, Chiu CF, Tsai MH, Chen CS. A potent indole-3-carbinol derived antitumor agent with pleiotropic effects on multiple signaling pathways in prostate cancer cells. Cancer Res. 2007 Aug
15;67(16):7815-24.
3.) Pappa G, Strathmann J, Löwinger M, Bartsch H, Gerhäuser C. Quantitative combination effects between sulforaphane and 3,3′-diindolylmethane on proliferation of human colon cancer cells in vitro. Carcinogenesis. 2007 Jul;28(7):1471-7. Epub 2007 Feb 28.
4.) Pappa G, Lichtenberg M, Iori R, Barillari J, Bartsch H, Gerhäuser C. Comparison of growth inhibition profiles and mechanisms of apoptosis induction in human colon cancer cell lines
by isothiocyanates and indoles from Brassicaceae. Mutat Res. 2006 Jul 25;599(1-2):76-87. Epub 2006 Feb 24.
5.) Bhuiyan MM, Li Y, Banerjee S, Ahmed F, Wang Z, Ali S, Sarkar FH. Down-regulation of androgen receptor by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in both hormone-sensitive LNCaP and insensitive C4-2B prostate cancer cells. Cancer Res. 2006 Oct 15;66(20):10064-72.
6.) Aggarwal BB, Ichikawa H. Molecular targets and anticancer potential of indole-3-carbinol and its derivatives. Cell Cycle. 2005 Sep;4(9):1201-15. Epub 2005 Sep 6.
7.) Chinni SR, Li Y, Upadhyay S, Koppolu PK, Sarkar FH. Indole-3-carbinol (I3C) induced cell growth inhibition, G1 cell cycle arrest and apoptosis in prostate cancer cells. Oncogene. 2001
May 24;20(23):2927-36.
8.) Cover CM, Hsieh SJ, Cram EJ, et al. Indole-3-carbinol and tamoxifen cooperate to arrest the cell cycle of MCF-7 human breast cancer cells. Cancer Res 1999;59:1244–51.

Lycopene

1.) Parsons JK, Newman VA, Mohler JL, Pierce JP, Flatt S, Marshall J. Dietary modification in patients with prostate cancer on active surveillance: a randomized, multicentre feasibility study. BJU Int. 2008 Jan 24 [Epub ahead of print].
2.) Wang A, Zhang L.[Effect of lycopene on proliferation and cell cycle of hormone refractory prostate cancer PC-3 cell line]. Wei Sheng Yan Jiu. 2007 Sep;36(5):575-8.
3.) Gunasekera RS, Sewgobind K, Desai S, Dunn L, Black HS, McKeehan WL, Patil B. Lycopene and lutein inhibit proliferation in rat prostate carcinoma cells. Nutr Cancer. 2007;58(2):171-7.
4.) Vaishampayan U, Hussain M, Banerjee M, Seren S, Sarkar FH, Fontana J, Forman JD, Cher ML, Powell I, Pontes JE, Kucuk O. Lycopene and soy isoflavones in the treatment of prostate cancer. Nutr Cancer. 2007;59(1):1-7.
5.) Zhang J, Dhakal I, Stone A, Ning B, Greene G, Lang NP, Kadlubar FF. Plasma carotenoids and prostate cancer: a population-based case-control study in Arkansas. Nutr Cancer. 2007;59(1):46-53.
6.) Hwang ES, Bowen PE. Effects of lycopene and tomato paste extracts on DNA and lipid oxidation in LNCaP human prostate cancer cells. Biofactors. 2005;23(2):97-105.
7.) Hantz HL, Young LF, Martin KR. Physiologically attainable concentrations of lycopene induce mitochondrial apoptosis in LNCaP human prostate cancer cells. Exp Biol Med (Maywood). 2005 Mar;230(3):171-9.
8.) Giovannucci E, Rimm EB, Liu Y, Stampfer MJ, Willett WC. A prospective study of tomato products, lycopene, and prostate cancer risk. J Natl Cancer Inst. 2002 Mar 6;94(5):391-8.
9.) Levy J, Bosin E, Feldman B, et al. Lycopene is a more potent inhibitor of human cancer cell proliferation than either a-carotene or ß-carotene. Nutr Cancer 1995;24:257–66.
10.) Giovannucci E. Tomatoes, tomato-based products, lycopene, and cancer: review of the epidemiologic literature. J Natl Cancer Inst 1999;91:317–31.

Larch arabinogalactin

1.) Sathisha UV, Jayaram S, Harish Nayaka MA, Dharmesh SM. Inhibition of galectin-3 mediated cellular interactions by pectic polysaccharides from dietary sources. Glycoconj J. 2007 Nov;24(8):497-507. Epub 2007 May 25.
2.) Choi EM, Kim AJ, Kim YO, Hwang JK. Immunomodulating activity of arabinogalactan and fucoidan in vitro. J Med Food. 2005 Winter;8(4):446-53.
3.) Larch arabinogalactan. Altern Med Rev. 2000 Oct;5(5):463-6. [NO AUTHORS LISTED].
4.) Kelly GS. Larch arabinogalactan: clinical relevance of a novel immune-enhancing polysaccharide. Altern Med Rev. 1999 Apr;4(2):96-103.
5.) Hagmar B, Ryd W, Skomedal H.Arabinogalactan blockade of experimental metastases to liver by murine hepatoma. Invasion Metastasis. 1991;11(6):348-55.
6.) Beuth J, et al.. Inhibition of liver tumor cell colonization in two animal tumor models by lectin blocking with D-galactose or arabinogalactan. Clin Exp Metastasis 1988;6:115–20.
7.) Hirai O, Fujitsu T, Mori J, Kikuchi H, Koda S, Fujioka M, Morimoto Y. Antitumour activity of purified arabinogalactan-peptidoglycan complex of the cell wall skeleton of
Rhodococcus lentifragmentus. J Gen Microbiol. 1987 Feb;133(2):369-73.

Modified Citrus Pectin

1.) Sathisha UV, Jayaram S, Harish Nayaka MA, Dharmesh SM. Inhibition of galectin-3 mediated cellular interactions by pectic polysaccharides from dietary sources. Glycoconj J. 2007
Nov;24(8):497-507. Epub 2007 May 25.
2.) Jackson CL, Dreaden TM, Theobald LK, Tran NM, Beal TL, Eid M, Gao MY, Shirley RB, Stoffel MT, Kumar MV, Mohnen D. Pectin induces apoptosis in human prostate cancer cells: correlation of apoptotic function with pectin structure. Glycobiology. 2007 Aug;17(8):805-19. Epub 2007 May 19.
3.) Chen CH, Sheu MT, Chen TF, Wang YC, Hou WC, Liu DZ, Chung TC, Liang YC. Suppression of endotoxin-induced proinflammatory responses by citrus pectin through blocking LPS signaling pathways. Biochem Pharmacol. 2006 Oct 16;72(8):1001-9. Epub 2006 Aug 22.
4.) Glinskii OV, Huxley VH, Glinsky GV, Pienta KJ, Raz A, Glinsky VV.Mechanical entrapment is insufficient and intercellular adhesion is essential for metastatic cell arrest in distant organs.
Neoplasia. 2005 May;7(5):522-7.
5.) Guess BW, Scholz MC, Strum SB, Lam RY, Johnson HJ, Jennrich RI. Modified citrus pectin (MCP) increases the prostate-specific antigen doubling time in men with prostate cancer: a phase II pilot study. Prostate Cancer Prostatic Dis. 2003;6(4):301-4.
6.) Pratima Nangia-Makker, Victor Hogan, Yuichiro Honjo, Sara Baccarini, Larry Tait, Robert Bresalier, Avraham Raz. Inhibition of Human Cancer Cell Growth and Metastasis in Nude Mice by Oral Intake of Modified Citrus Pectin. J Natl Cancer Inst, Vol. 94, No. 24, December 18, 2002
7.) Nangia-Makker P, Hogan V, Honjo Y, Baccarini S, Tait L, Bresalier R, Raz A. Inhibition of human cancer cell growth and metastasis in nude mice by oral intake of modified citrus pectin. J Natl Cancer Inst. 2002 Dec 18;94(24):1854-62.
8.) Pienta KJ, Naik H, Akhtar A, Yamazaki K, Replogle TS, Lehr J, et al. Inhibition of spontaneous metastasis in a rat prostate cancer model by oral administration of modified citrus pectin. J Natl Cancer Inst 1995;87:348–53.
9.) Hsieh TC, Wu JM. Changes in cell growth, cyclin/kinase, endogenous phosphoproteins and nm23 gene expression in human prostatic JCA-1 cells treated with modified citrus pectin. Biochem Mol Biol Int. 1995 Nov;37(5):833-41.
10.) Platt D, Raz A. Modulation of the lung colonization of B16-F1 melanoma cells by citrus pectin. J Natl Cancer Inst. 1992 Mar 18;84(6):438-42.

 

CANCER PREVENTION

Natural Strategies To Help Avoid Cancer

What is Cancer?
The word “cancer” is a general term used to describe body cells that grow uncontrollably and often invade other body tissue. Benign tumors are also body cells that multiply, but they do not grow uncontrollably and invade other parts of the body. Cancer can begin in virtually any part of the body. The most common locations for cancer are the lungs, colon, breast, and prostate.

How does Cancer start?
Scientists believe that cancer starts as a single cell with altered chromosomes. Chromosomes are the “brain” inside each cell in the body. Chromosomes tell the cell how to behave.

In cancer cells, abnormal chromosomes give rise to abnormal cell behavior. Such abnormal behavior includes rapid multiplication of cells. Unlike normal cells, cancer cells do not stop growing when they reach a particular number. Instead, they continue to multiply, pushing on vital organs, robbing the “host” of nutrients, and spreading to other parts of the body by way of the lymphatic or blood-vascular system. (A process called “metastasis”).

What Causes Cancer?
Altered chromosomes inside the cell are ultimately thought to be responsible for abnormal cell behavior. But what causes chromosomes to become altered?

A number of factors are known to alter chromosomes. Some of these alterations may be pre-programmed into a cell; what we would call “genetic.” A person may be born with such abnormal chromosomes.

Other factors that are known to damage chromosomes and initiate cancer are known as carcinogens. These appear to be a far more common cause of cancer. Carcinogenic substances include ionizing radiation, smoke, and a wide variety of chemicals. Chronic irritation of any body tissue can also cause a cell to become cancerous.

Cancer and the Immune System
Scientists have demonstrated that a normal body produces approximately 300 or more cancerous cells per day. So why doesn’t everyone develop cancer? The answer lies in the immune system, a portion of the body that is designed to protect us from foreign “invasion.” In a body with a healthy immune system, cancer cells are recognized and destroyed. This process occurs inside everyone, all the time, every day. When the immune system is “compromised’ for any reason – for example, from nutritional deficiencies, cigarette smoking, or excessive physical or emotional stress – it may fail to identify cancerous cells. Once a cancerous cell begins to multiply, it becomes more difficult for the immune system to contain it. (Think of a wild fire. Very early, it is easy to put out. Let it “grow” for a while, and it becomes more dangerous).

Diagnosis of Cancer
There is no early blood or other tests that will tell us when an aberrant cell has escaped immune system recognition. In fact, our current diagnosis of cancer usually relies on a “mass,” or noticeable tumor, being present. Mammography, a low dose X-ray picture taken of the female breast, is an example of an early detection method. Though often touted as “prevention,” it is not. Diagnostic test are a means of early detection of cancer. They are NOT preventive measures.

The “War on Cancer”
President Nixon signed a bill on December 23, 1971, declaring an all-out “war” on cancer. This bill opened a floodgate of federal funding to research a cure for cancer. Since the signing of this bill, tens of billions of dollars of federal money, and additional private sector money, have been spent on this “war on cancer.”

Don’t let anyone fool you: it’s a “war” we’re losing. Since the signing of this bill, the death rate from cancer has risen. Some people will tell you these statistics are inaccurate because people are living longer, but this, too, is a falsehood. These numbers are age adjusted.

Common cancers, such as lung cancer, are increasingly common. Prostate and brain cancers and non-Hodgkin’s lymphoma are beginning to rise in the general population. So are a number of other types of cancer.

Conventional Treatment of Cancer
Like the stories that suggest that we are winning the “war on cancer,” conventional treatment improvements are a myth. There has been little significant advancement in the treatment of cancer in the past twenty years.

What has improved is our ability to detect cancer earlier, when it is still curable by surgery alone. Radiation and chemotherapy can provide a margin of additional “time” in a few types of cancer, but often at the expense of quality of life.

Surgery still remains one of the best conventional treatments for cancer, and then, it is most effective when the cancer is detected early. Surgery is also more effective when the immune system is otherwise strong and healthy.

Don’t misunderstand me. There are some advances in survival times with the use of certain drugs. For example, the anti-estrogen drug Tamoxifen improves survival times in post menopausal women with hormone-responsive breast cancer. Of course, if these women were “stage I” or “stage II’ when their cancer was removed, the chance of recurrence of cancer is very low anyway. Again, this is an indication that early detection and surgical removal remains one of our most effective conventional treatments. Certain nutritional supplements should sometimes be avoided during chemotherapy because they can reduce the effectiveness of the drugs, but most supplements actually minimize negative side-effects of chemotherapy and radiation. And there are some types of cancers that, although present in a body, should probably be left alone because they are unlikely to spread.

All of these questions need to be answered with the assistance of an holistic physician who can help you determine the best course of action to take and will work with you to sort out the legitimate treatments from the “hype.” There is no room for guesswork and inexperience once a diagnosis of cancer has been made. Please consider obtaining a consultation with Dr. Myatt.

Prevention is the Best “Cure”
Modern medical science may not know much more about treating cancer than it did twenty years ago, but we do know a lot more about prevention. At this point in medical history, it’s fair to say that prevention of cancer is a surer and safer bet than cure.

DIET AND LIFESTYLE RECOMMENDATIONS

  • Maintain a normal weight. Excess body fat is associated with a number of cancers, including postmenopausal breast cancer and prostate cancer.
  • Eat a diet rich in antioxidant nutrient foods (fruits and vegetables). Include “Super Foods” lavishly. Use soy and soy products if tolerated. Buy organic produce whenever possible.
  • Do not smoke. Limit alcohol consumption.
  • Drink pure water, not tap water. Chlorine byproducts are can cause urinary tract and other cancers. Other contaminants in water have unknown effects but many are believed to relate to cancer.
  • Exercise regularly. Many types of cancers (ovarian, breast, prostate, colon) occur far less often (up to 50% less) in people who engage in regular physical activity. [Ref.: N. Eng. J. Med. 338:94,1998]
  • Practice “Emotional hygiene.” Emotional distress (“stress”) suppresses the immune system and may make a person more susceptible to cancer and other diseases. Conversely, optimism is associated with improved immunity in a number of studies. Watch The Body/Mind Connection video to learn exactly how this occurs.

 

PRIMARY SUPPORT:

 

  • Maxi Multi: 3 caps, 3 times per day with meals. Optimal (not minimal) doses of all nutrients are important in preventing cancer, since a single micronutrient deficiency can cause immune system weakness. Antioxidants (A, C, carotene and selenium), and vitamin D are especially important.
  • Maxi Greens: 3 caps, 3 times daily with meals for complete phytonutrient coverage.
  • Omega 3 fatty acids:
    Flax seed meal, 2 teaspoons per day with food
    OR
    Flax seed capsules
    : 2-4 caps, 3 times per day (target dose range: 6-12 caps per day)
    OR
    Flax seed oil
    : 1-2 tablespoons per day
    OR
    Max EPA
    (Omega-3 rich fish oil): 1-2 caps, 3 times per day with meals (target dose: 3-6 caps per day).

 

ADDITIONAL SUPPORT

 


References

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Super Foods

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Smoking, Alcohol and Cancer Risk

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Drinking Water and Cancer Risk

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Exercise and Cancer

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Emotional Hygiene and The immune System

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Multiple Vitamins and Cancer

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Antioxidants (General) and Cancer

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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.

Vitamin D

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

Omega 3 Essential Fatty Acids

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

Di-indolymethanes (DIM, IC3)

1.) Moiseeva EP, Almeida GM, Jones GD, Manson MM.Extended treatment with physiologic concentrations of dietary phytochemicals results in altered gene expression, reduced growth, and apoptosis of cancer cells. Mol Cancer Ther. 2007 Nov;6(11):3071-9.
2.) Weng JR, Tsai CH, Kulp SK, Wang D, Lin CH, Yang HC, Ma Y, Sargeant A, Chiu CF, Tsai MH, Chen CS. A potent indole-3-carbinol derived antitumor agent with pleiotropic effects on multiple signaling pathways in prostate cancer cells. Cancer Res. 2007 Aug 15;67(16):7815-24.
3.) Pappa G, Strathmann J, Löwinger M, Bartsch H, Gerhäuser C. Quantitative combination effects between sulforaphane and 3,3′-diindolylmethane on proliferation of human colon cancer cells in vitro. Carcinogenesis. 2007 Jul;28(7):1471-7. Epub 2007 Feb 28.
4.) Pappa G, Lichtenberg M, Iori R, Barillari J, Bartsch H, Gerhäuser C. Comparison of growth inhibition profiles and mechanisms of apoptosis induction in human colon cancer cell lines by isothiocyanates and indoles from Brassicaceae. Mutat Res. 2006 Jul 25;599(1-2):76-87. Epub 2006 Feb 24.
5.) Bhuiyan MM, Li Y, Banerjee S, Ahmed F, Wang Z, Ali S, Sarkar FH. Down-regulation of androgen receptor by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in both hormone-sensitive LNCaP and insensitive C4-2B prostate cancer cells. Cancer Res. 2006 Oct 15;66(20):10064-72.
6.) Aggarwal BB, Ichikawa H. Molecular targets and anticancer potential of indole-3-carbinol and its derivatives. Cell Cycle. 2005 Sep;4(9):1201-15. Epub 2005 Sep 6.
7.) Chinni SR, Li Y, Upadhyay S, Koppolu PK, Sarkar FH. Indole-3-carbinol (I3C) induced cell growth inhibition, G1 cell cycle arrest and apoptosis in prostate cancer cells. Oncogene. 2001 May 24;20(23):2927-36.
8.) Cover CM, Hsieh SJ, Cram EJ, et al. Indole-3-carbinol and tamoxifen cooperate to arrest the cell cycle of MCF-7 human breast cancer cells. Cancer Res 1999;59:1244–51.

Turmeric (Curcumin)

1.) Ji C, Cao C, Lu S, Kivlin R, Amaral A, Kouttab N, Yang H, Chu W, Bi Z, Di W, Wan Y. Curcumin attenuates EGF-induced AQP3 up-regulation and cell migration in human ovarian cancer cells.Cancer Chemother Pharmacol. 2008 Jan 23 [Epub ahead of print].
2.) Steward WP, Gescher AJ. Curcumin in cancer management: Recent results of analogue design and clinical studies and desirable future research. Mol Nutr Food Res. 2008 Jan 9 [Epub ahead of print].
3.) Shankar S, Ganapathy S, Chen Q, Srivastava RK. Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis and angiogenesis. Mol Cancer. 2008 Jan 29;7(1):16 [Epub ahead of print]
4.) Moiseeva EP, Almeida GM, Jones GD, Manson MM. Extended treatment with physiologic concentrations of dietary phytochemicals results in altered gene expression, reduced growth, and apoptosis of cancer cells. Mol Cancer Ther. 2007 Nov;6(11):3071-9.
5.) Shankar S, Chen Q, Sarva K, Siddiqui I, Srivastava RK. Curcumin enhances the apoptosis-inducing potential of TRAIL in prostate cancer cells: molecular mechanisms of apoptosis, migration and angiogenesis. J Mol Signal. 2007 Oct 4;2:10.
6.) Shankar S, Srivastava RK. Bax and Bak genes are essential for maximum apoptotic response by curcumin, a polyphenolic compound and cancer chemopreventive agent derived from turmeric, Curcuma longa. Carcinogenesis. 2007 Jun;28(6):1277-86. Epub 2007 Feb 2.
7.) Shankar S, Srivastava RK. Involvement of Bcl-2 family members, phosphatidylinositol 3′-kinase/AKT and mitochondrial p53 in curcumin (diferulolylmethane)-induced apoptosis in prostate cancer. Int J Oncol. 2007 Apr;30(4):905-18.
8.) Somers-Edgar TJ, Scandlyn MJ, Stuart EC, Le Nedelec MJ, Valentine SP, Rosengren RJ. The combination of epigallocatechin gallate and curcumin suppresses ERalpha-breast cancer cell growth in vitro and in vivo. Int J Cancer. 2007 Dec 20 [Epub ahead of print].
9.) Chen A, Xu J, Johnson AC. Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1. Oncogene. 2006 Jan 12;25(2):278-87.
10.) Wahl H, Tan L, Griffith K, Choi M, Liu JR. Curcumin enhances Apo2L/TRAIL-induced apoptosis in chemoresistant ovarian cancer cells. Gynecol Oncol. 2007 Apr;105(1):104-12. Epub 2006 Dec 15.
11.) Chen J, Wanming D, Zhang D, Liu Q, Kang J.Water-soluble antioxidants improve the antioxidant and anticancer activity of low concentrations of curcumin in human leukemia cells. Pharmazie. 2005 Jan;60(1):57-61.
12.) Deeb DD, Jiang H, Gao X, Divine G, Dulchavsky SA, Gautam SC. Chemosensitization of hormone-refractory prostate cancer cells by curcumin to TRAIL-induced apoptosis. J Exp Ther Oncol. 2005;5(2):81-91.
13.)Dobrovolskaia MA, Kozlov SV.: Inflammation and cancer: when NF-kappaB amalgamates the perilous partnership. Curr Cancer Drug Targets. 2005 Aug;5(5):325-44.
14.) Deeb D, Jiang H, Gao X, Hafner MS, Wong H, Divine G, Chapman RA, Dulchavsky SA, Gautam SC. Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing gand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation. Mol Cancer Ther. 2004 Jul;3(7):803-12.
15.) Van Erk MJ, Teuling E, Staal YC, Huybers S, Van Bladeren PJ, Aarts JM, Van Ommen B. Time- and dose-dependent effects of curcumin on gene expression in human colon cancer cells. J Carcinog. 2004 May 12;3(1):8.
16.)Ernst P.: The role of inflammation in the pathogenesis of gastric cancer. Aliment Pharmacol Ther. 1999 Mar;13 Suppl 1:13-8
17.) Menon LG, Kuttan R, Kuttan G. Anti-metastatic activity of curcumin and catechin. Cancer Lett 1999;141:159–65.
18.) Khafif A, Schantz SP, Chou TC, Edelstein D, Sacks PG. uantitation of chemopreventive synergism between (-)-epigallocatechin-3-gallate and curcumin in normal, premalignant and malignant human oral epithelial cells. Carcinogenesis. 1998

Melatonin

1.) Lissoni P, Barni S, Mandalà, et al. Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal hormone melatonin in metastatic solid tumour patients with poor clinical status. Eur J Cancer 1999;35:1688–92.
2.) Lissoni P, Cazzanga M, Tancini G, et al. Reversal of clinical resistance to LHRH analogue in metastatic prostate cancer by the pineal hormone melatonin: efficacy of LHRH analogue plus melatonin in patients progressing on LHRH analogue alone. Eur Urol 1997;31:178–81.
3.) Lissoni P, Paolorossi F, Tancini G, et al. Is there a role for melatonin in the treatment of neoplastic cachexia? Eur J Cancer 1996;32A:1340–3.
4.) Lissoni P, Paolorossi F, Tancini G, et al. A phase II study of tamoxifen plus melatonin in metastatic solid tumour patients. Br J Cancer 1996;74:1466–8.
5.) Lissoni P, Brivio O, Brivio F, et al. Adjuvant therapy with the pineal hormone melatonin in patients with lymph node relapse due to malignant melanoma. J Pineal Res 1996;21:239–42.
6.) Lissoni P, Barmo S. Meregalli S, et al. Modulation of cancer endocrine therapy by melatonin: a phase II study of tamoxifen plus melatonin in metastatic breast cancer patients progressing under tamoxifen alone. Br J Cancer 1995;71:854–6.
7.) Reiter RJ, Melchiorri D, Sewerynek E, Poeggeler B, Barlow-Walden L, Chuang J, Ortiz GG, Acuna-Castroviejo D.: A review of the evidence supporting melatonin’s role as an antioxidant.J Pineal Res. 1995 Jan;18(1):1-11.
8.) Neri B, Fiorelli C, Moroni F, et al. Modulation of human lymphoblastoid interferon activity by melatonin in metastatic renal cell carcinoma. Cancer 1994;73:315–9.
9.) Lissoni P, Barni S, Cazzaniga M, Ardizzoia A, Rovelli F, Brivio F, Tancini G.: Efficacy of the concomitant administration of the pineal hormone melatonin in cancer immunotherapy with low-dose IL-2 in patients with advanced solid tumors who had progressed on IL-2 alone. Oncology. 1994 Jul-Aug;51(4):344-7.
10.) Lissoni P, Barni S, Ardizzoia A, et al. A randomized study with the pineal hormone melatonin versus supportive care alone in patients with brain metastases due to solid neoplasms. Cancer 1994;73:699–701.
11.) Lissoni P, Barni S, Tancini G, et al. A randomised study with subcutaneous low-dose interleukin 2 alone vs interleukin 2 plus the pineal neurohormone melatonin in advanced solid neoplasms other than renal cancer and melanoma. Br J Cancer 1994;69:196–9.
12.) Aldeghi R, Lissoni P, Barni S, et al. Low-dose interlekin-2 subcutaneous immunotherapy in association with the pineal hormone melatonin as a first-line therapy in locally advanced or metastatic hepatocellular carcinoma. Eur J Cancer 1994;30A:167–70.
13.) Lissoni P, Brivio F, Ardizzoia A, et al. Subcutaneous therapy with low-dose interlekin-2 plus the neurohormone melatonin in metastatic gastric cancer patients with low performance status. Tumori 1993;79:401–4.
14.) Lissoni P, Barni S, Ardizzoia A, et al. Randomized study with the pineal hormone melatonin versus supportive care alone in advanced nonsmall cell lung cancer resistant to a first-line chemotherapy containing cisplatin. Oncology 1992;49:336–9.
15.) Lissoni P, Barni S, Crispino S, et al. Endocrine and immune effects of melatonin therapy in metastatic cancer patients. Eur J Cancer Clin Oncol 1989;25:789–95.

Candidiasis (Chronic)

Natural Strategies Yeast Overgrowth

Everyone carries the common yeast Candida albicans in their intestinal tract. Other strains of Candida may also inhabit the colon. Yeasts are normal but apparently non-essential residents of the large intestine. Sometimes, these co-inhabitants of the intestinal tract can grow out of control.

An overgrowth of yeast can cause many problems. The yeasts release waste products that, when absorbed into the blood stream, are toxic to many body systems. These byproducts can be recognized by the immune system and create and immune reaction.

Candida overgrowth results from conditions inherent to modern life: use of antibiotics and other drugs, a Standard American Diet (S.A.D. – especially sugar and simple carbohydrates), a lack of digestive enzymes, and stress. Overuse or misuse of antibiotics is another common cause of Candida overgrowth.

The Elusive Diagnosis

The diagnosis of Candidiasis is often overlooked in conventional medicine. Many doctors say they “Don’t believe in Candidiasis,” even though there is ample scientific evidence to document the condition. It is difficult to say exactly why this condition is ignored by conventional medicine in spite of the vast scientific evidence, but I offer you my theories for such conventional medical ignorance:

  • The symptoms of Candidiasis are widespread and can mimic many other diseases. There is no definitive lab test that confirms the disease. This makes correct diagnosis difficult.
  • Some “holistic” practitioners diagnose everything as Candidiasis, thereby missing other important diagnoses. This has given the problem of Candidiasis a “pop diagnosis” reputation among many physicians. As a result, non-holistic doctors are then reluctant to recognize true cases of Candidiasis.
  • One of the primary causes of Candidiasis is the overuse and inappropriate use of antibiotics, steroids, birth control pills and other drugs. To acknowledge Candidiasis as a disease is to also acknowledge a problem often caused by drugs!

Symptoms of Candidiasis

Toxins absorbed from Candida can affect any tissue. Those systems most commonly affected include the gastrointestinal (GI), genito-urinary (GU), nervous, and immune systems. A person suffering from Candidiasis may have any of these symptoms:

  • In the intestinal tract: bloating, excessive feeling of fullness, diarrhea, constipation, alternating diarrhea and constipation, “rolling gas,” abdominal cramping, heartburn, indigestion, gas or belching, mucous in the stool, hemorrhoids.
  • In the female genital tract: recurrent yeast vaginitis, persistent vaginal itching or burning, persistent vaginal discharge, endometriosis, PMS.
  • In the male genital tract: prostatitis, impotence, loss of sexual desire.
  • In the urinary tract: urgency or urinary frequency, recurrent urinary tract “infections” but bacteria are NOT found to be the cause.
  • In the nervous system: numbness, burning, or tingling, spots in front of the eyes, erratic vision, incoordination, irritability or jitteriness, dizziness or loss of balance, failing vision, ear pain or deafness.
  • In the immune system: rashes, post nasal drip, sore or dry throat, wheezing or shortness of breath, recurrent infections, burning or tearing of eyes, cough.
  • In the skin and mucous membranes: recurrent skin fungal infections, nail-bed fungus, “jock itch,” thrush (yeast overgrowth in the mouth and esophagus), psoriasis, rashes of unknown origin.
  • In general: fatigue, mental “cloudiness,” joint aches and pains, obesity, depression, memory loss.

How Is Candida diagnosed?

Symptoms of Candida overgrowth suggest the diagnosis. In addition, other causes of a complaint must be “ruled out.” For example, if a patient complains of extreme fatigue, we would first determine that this complaint was NOT caused by other factors, such as anemia, low thyroid function, or viral infection. When other known causes of fatigue have been ruled out, especially if the patient has additional symptoms or history that suggest Candida overgrowth, further testing for Candidiasis is warranted. Treatment can be started “presumptively,” (meaning before we are sure of Candida overgrowth).

Personal history also suggests the diagnosis. Antibiotic use without bacterial replacement therapy, birth control pills, cortisone therapy, and a history of dietary imbalance (especially sugar, simple carbohydrate or alcohol use or cravings) are also indicators.

A Candida stool test can aid in the diagnosis and guide treatment. Since yeast is a normal inhabitant in everyone’s intestinal tract, some amount of yeast can almost always be recovered in a stool sample. Only when recovered amounts are abnormally high is the diagnosis clear. Because Candida can “invade” directly into the tissue of the GI tract, it is possible to have a Candidal overgrowth but a “normal” amount of yeast in the stool. Since a lack of normal bowel bacteria OR an increase in abnormal bowel bacteria often accompanies yeast overgrowth, a Gastro-intestinal health profile with parasitology is often more useful for diagnosis than the Candida stool test alone.

A Candida Antibodies Test is also available. This test uses a drop of blood to evaluate for an immune system reaction to Candida. It assesses IgG, IgA, IgM immunoglobulins to yeast as well as Candida antigen. A positive finding indicates past or present Candida infection and may allow Candida yeast reactions to be found when stool and vaginal specimens are negative or inconclusive.

Careful consideration of a patient’s symptoms, “ruling out” other known causes of the complaint, evaluation of dietary and drug history, and use of laboratory tests are the way that Candidiasis is accurately diagnosed. Diagnosis can be challenging because Candidiasis shares symptoms with many other conditions. For this reason, it is recommended that you consult an holistic physician for correct diagnosis and treatment.

What is the Treatment?

Cessation of the causative factors is most important. Whether it be a particular drug, a high sugar/refined carbohydrate diet, or an excess response to external events (more commonly known as “stress”), these triggers must be corrected. An anti-yeast substance with concomitant bacterial replacement therapy, corrective diet, stress reduction and immune system boosting are all crucial to the success of the treatment. Your holistic physician will be able to help you determine your best course of action in treating this modern-day “plague.”

Yeast “Die-Off”: Avoiding the Herxheimer Reaction

Yeast cells that are quickly killed by treatment cause a “die-off” reaction known as the Herxheimer reaction. Die-off is caused by the release of large amounts of toxins from dying Candida cells. These toxins pass through the gut wall and enter the bloodstream where they can trigger immune reactions. Die-off reactions can last from a few days to several weeks but usually clear up in less than a week.

In order to avoid die-off reactions, I recommend high doses of activated charcoal and plenty of fluids. The charcoal adsorbs the killed yeast cells and their toxic waste products and carries them out of the body in the stool before they are absorbed into the bloodstream and can create a Herxheimer reaction.

Diet And Lifestyle Recommendations

  • Avoid ALL foods that are high in simple carbohydrates (sugar, corn syrup, honey, molasses, fruit juice, dried fruit, other sugars or foods containing them), yeasts (all raised, yeasted dough: bread, crackers, bagels), ferments and molds (mushrooms, alcohol, vinegar, peanuts, cantaloupe), milk products except yogurt (milk is high in the sugar lactose), high carbohydrate vegetables (potatoes, corn, parsnip). Eat “Super Foods” plentifully, especially fresh garlic.
  • Avoid all known food allergens (see Food Allergies).
  • Avoid antibiotics, birth control pills, steroids, immune suppressing drugs unless absolutely medically necessary. (Do NOT stop medications without physician guidance).

Primary Support

  • Maxi Multi: A deficiency of any vitamin, mineral or trace mineral can weaken this immunity and predispose to Candida overgrowth. For this reason, a high potency multiple vitamin/mineral/trace mineral formula is a critical first step in treating Candida. Be SURE that only yeast-free, hypoallergenic supplements are used. Maxi Multi is yeast and additive-free and hypoallergenic. Dose: 3 caps, 3 times per day with meals.
  • Similase: digestive enzymes reduce bowel inflammation, improve digestion which in turn nourishes normal gut flora (good bacteria) and decreases yeast die-off reaction. Dose: 1-2 caps, 3 times per day with meals.
  • Berberine: Highly effective against candida. Dose: one capsule two times daily for up to fourteen (14) days with water at mealtimes
  • Activated Charcoal: charcoal binds toxins released as yeast dies. This prevents them from being reabsorbed into circulation and carries them out in the stool. Charcoal is especially good for preventing the “Herxheimer Reaction” (yeast die-off, see above).
    Charcoal capsules: Dose: 12 capsules 2 times per day, once between breakfast and lunch and once at bedtime with a full glass of water.
  • Suprema-Dophilus (Ultra high-potency probiotic): Replacement of normal “good bacteria” helps crowd out yeast and prevent their recurrence. Note that many probiotic formulas are not enteric coated and therefore do not survive stomach acid before making their way to the colon. SupremaDophilus is enteric coated to insure proper delivery to the colon. Dose: 1 cap before bed.
  • 35 Billion ProBiotic is “Supremadophilus on Steroids” – Sometimes, bigger really is better. Our new super-high-potency Supremadophilus has 35 billion viable probiotics compared to 5 billion in Supremadophilus. Recommended during and after antibiotic treatment and for those times when a more vigorous gut bacterial replacement is indicated. Dose: one capsule per day at bedtime or as directed.
  • Immune Support: Dose: 2 caps, 2 times per day with meals

TopicalTreatments

  • Tea Tree oil: Essential oil of tea tree can be used on skin and nails for fungal infections. Tea tree oil may be used in water as a douche for yeast vaginitis.

Tests

  • Candida stool test. A culture can be done by a specialized lab to determine which anti-yeast herbs or drugs will be more effective.
  • CANDIDA ANTIBODIES: Low-level overgrowth of Candida yeast species can cause a wide variety of health problems, but yeast may not be found in a stool specimen. This is because the yeast may have invaded elsewhere in the body, such as in the urinary tract, sinus passages, vagina or elsewhere.
    This test uses a drop of blood to evaluate for an immune system reaction to Candida. It assesses IgG, IgA, IgM immunoglobulins to yeast as well as Candida antigen. A positive finding indicates past or present Candida infection and may allow Candida yeast reactions to be found when stool and vaginal specimens are negative or inconclusive.
  • Gastro-intestinal health profile with parasitology is often more useful for diagnosis than the Candida stool test alone because it also examines normal and abnormal gut bacteria and parasites.

Cataracts

Prevent and Possibly Reverse Lens Opacity

Cataracts are an opacity of the eye lens which gives a visual sensation like trying to look through a cloudy window. In their early stages, cataracts may not be much of a problem. As they progress, however, it can become more difficult, or even impossible, to see clearly. Cataracts are the leading cause of decreased vision in adults over age 65, and cataract surgery is the most common surgical procedure for seniors.

People can get have “age-related” cataracts in their 40s or 50s, though the changes at this stage tend to be small and vision disturbance minimal. By age 55, 15% of people have cataracts. This figure jumps to 50 percent by age 75, and 90 percent by age 85. It’s important to note, however, that cataracts worsen over time … so it’s never too late-or early-to try to prevent them and/or treat them!

Causes of Cataracts

The lens of the eye is made of largely of protein and water. Most of the cells in our body are replaced by new cells over time. However, cells in the lens of the eye have no such “turnover.” The lens that you are born with is the same lens that you will have for the rest of your life.

Light normally passes through the lens of the eye without distortion, as if the lens were made of clear glass. When the lens becomes is injured, proteins within the eye begin to “clump.” This clumping of lens protein results in the characteristic “cloudiness.”

Factors that damage the lens include high exposure to UV-B light, oxidative stress from free radicals, nutrient deficiencies, high blood sugar levels, exposure to radiation, prolonged intake of corticosteroid or other drugs, and cigarette smoking.  Fortunately, these factors are all controllable.

Other less common causes of cataracts include infection and eye injury. There is also a form of congenital cataracts which affects infants and young children.

Cataract Prevention

UV-B radiation from sunlight is thought to be one of the leading causes of cataracts. Wearing UV-B protective sunglasses is a simple way to minimize the damaging effects of UV-B. [Dr. Myatt’s Note: I personally do not believe that sunlight per se is the cause of cataracts. After all, humans have been running around without sunglasses for thousands of years without going blind from cataracts. Could it be that low levels of anti-oxidants, as discussed in the next paragraph, predispose to sunlight damage? Or the decreased protection of the ozone layer that ordinarily filters out UV-B light? Until more is known, I still wear my sunglasses when I’m outdoors for extended periods].

The second known cause of cataract formation is free radical damage to the lens. This free radical damage is associated with a deficiency of anti-oxidant nutrients in the diet. Studies have shown that people with higher intakes of vitamins A,C,E, carotenes (especially lutein and zeanthin) have significantly lower rates of cataracts. In animals, grape seed extract (which is 50 times more potent in antioxidant properties than vitamin C and E) prevented cataracts in rats that had genetic tendencies to develop opacities.

In the large Beaver Dam Eye Study, scientists followed dietary intake of antioxidant nutrients and the incidence of cataract formation in a group of 1,354 adults, aged 43-84, for a period of over seven years. People who ate the most foods high in anti-oxidants had the lowest incidence of cataracts. The researchers concluded that the results “are consistent with a possible protective influence of lutein and vitamins E and C on the development of . . . cataracts.”

In the Nurse’s Health Study, researchers followed 50,828 women, aged 45-67, for eight years. Women who consumed the most vitamin A had a 39% lower risk of developing cataracts than women who consumed the least vitamin A.

Bilberry and vitamin E are have been linked to an improvement in cataracts. In 25 patients with senile cataracts, a combination of bilberry, standardized to contain 25-percent anthocyanosides (180 mg twice per day), and vitamin E (100 mg twice per day) for four months stopped the progression of cataracts in 96 percent of the subjects  compared to 76 percent in the 25 subjects in the control group. In another trial, people who took vitamin E supplements had less than half the risk of developing cataracts, compared with others in the five-year study. A daily dose of  400 IU of vitamin E per day is typically recommended for prevention. Smaller amounts (approximately 50 IU per day) have offered no protection in double-blind studies.

Vitamin C levels in the eye are known to decrease with age. Supplementing with vitamin C can prevent this decrease and has been linked to a lower risk of developing cataracts. People who take multivitamins or other supplements containing vitamins C or E for more than 10 years have been reported to have a 60% lower risk of forming a cataract. In one  study, people taking vitamin C for at least ten years showed a dramatic reduction in cataract risk, but those taking vitamin C for less than ten years showed no evidence of protection.

Diets high in spinach and kale have been reported lower the risk for cataracts. Spinach and kale are high in lutein and zeaxanthin, (carotenoids similar to beta-carotene). Lutein is normally found in the lens of the eye. In another study,  people with the highest intakes of lutein and zeaxanthin were half as likely to develop cataracts as those with the lowest intake.

Can Cataracts be Reversed?

If you are experiencing early vision changes due to cataracts, or have been told during an eye exam that you have “early cataracts,” you already know the conventional medical treatment: “Let them ripen” and we’ll surgically remove them. (“Let them ripen” is doctor-speak for “let them get worse”).

While surgical removal of cataracts can surely be a blessing to people with advanced cataracts, some 20-30% of those who undergo cataract surgery develop a subsequent clouding of the lens capsule, the part of the lens left in the eye to hold the new synthetic lens in place. If the capsule becomes cloudy, additional surgery may be required to restore clear vision. In some cases the surgery can lead to serious complications such as swelling of the eye, infections, and even blindness. Obviously, prevention is easier and safer than surgical “cure.”

Although most of the studies have focused on prevention, several have looked at actually reversing already-existing cataracts.

In one study, supplementation with 15 mg of lutein three times a week for one year significantly improved visual function in a small group of people with age-related cataracts.

Studies conducted in Russia have shown moderate to marked improvement in lens opacity with continued use of eye drops containing N-Acety-l-Carnosine. It took three months of continuous use for measurable improvmenets, and at six months, improvement stabilized. Some of the studies report results as high as 100% of participants experiencing noticeable changes (for the better!) in their vision.

Since N-Acety-l-Carnosine eye drops are not “FDA approved” for use in cataracts, you will see the productslisted as “lubricating eye drops.”

Do they work? I don’t know. But there are enough studies with impressive reports that I would certainly consider using these drops for at least three months if I had any degree of cataracts.

DIET AND LIFESTYLE RECOMMENDATIONS

  • Eat a diet high in “Super Foods” and antioxidant nutrients.
  • Decrease carbohydrates and simple sugars in the diet. This is especially important for preventing diabetic cataracts. Sugars bind with body proteins to produce AGES (Advanced Glycosylated End-products) that cause irreversible changes in the lens of the eye.
  • Drink at least 64 ounces of pure water daily. The vitreous portion of the eye has a high water content.
  • Wear high UV protection sunglasses.
  • DON’T SMOKE! Smoking greatly accelerates the formation of cataracts.

PRIMARY SUPPORT

  • Maxi Multi: 3 caps, 3 times per day with meals. Optimal (not minimal) doses of antioxidants (ACES), carotenes, B complex vitamins, selenium, zinc and bioflavonoids are particularly important for eye health.
  • Maxi Greens (Advanced Phytonutrient Formula): 3 caps, 3 times per day with meals. Bilberry, grape seed extract and ginkgo are particularly important, but plant flavonoids in general help protect the eyes.
  • Dr. Myatt’s Eye Drops from Hell: rinse eyes 2-4 times per day according to instructions. This formula increases circulation to the eyes and is good for eye health in general.

ADDITIONAL SUPPORT

  • Lack of normal stomach acid (low gastric acid) and resultant failure to absorb nutrients from diet and supplementation can contribute to eye disease. I recommend a Gastric Acid Self-Test for anyone concerned about vision and eye health.
  • Lutein and Zeaxanthin 15 -20mg, 3 times per week. People with the highest intakes of these two carotenoids had only 1/2 the risk of developing cataracts as the general population. In one study, people who supplemented these carotendoids at the recommended dose has a significant improvement in age-related cataracts.
  • Bilberry extract: 1 cap, 2-3 times per day with meals (Target dose range: 120-240mg or more per day).

FOR POSSIBLE CATARACT REVERSAL OR IMPROVEMENT

  • Lutein and Zeaxanthin 15 -20mg, 3 times per week. People with the highest intakes of these two carotenoids had only 1/2 the risk of developing cataracts as the general population. In one study, people who supplemented these carotendoids at the recommended dose has a significant improvement in age-related cataracts.
  • N-Acety-l-Carnosine eye drops: 1-2 drops per day, 1-2 times daily.

References

1.) Procyanidin-rich extract from grape seeds prevents cataract formation in hereditary cataractous (ICR/f) rats. J Agric Food Chem. 2002 Aug 14;50(17):4983-8.

2.) Antioxidant intake and risk of incident age-related nuclear cataracts in the Beaver Dam Eye Study. Am J Epidemiol. 1999 May 1;149(9):801-9.

3.) Nutrient intake and cataract extraction in women: a prospective study. BMJ. 1992 Aug 8;305(6849):335-9.

4.) Preventive medical treatment of senile cataract with vitamin E and anthocyanosides: clinical evaluation. Ann Ottalmol Clin Ocul. 1989;115:109.

5.) Cataract: relationship between nutrition and oxidation. J Am Coll Nutr 1993;12:138–46 [review].

6.) Relationship in humans between ascorbic acid consumption and levels of total and reduced ascorbic acid in lens, aqueous humor, and plasma. Curr Eye Res 1991;10:751–9.

7.) Epidemiologic evidence of a role for the antioxidant vitamins and carotenoids in cataract prevention. Am J Clin Nutr 1991;53:352S–5S.

8.) Antioxidant status in persons with and without senile cataract. Arch Ophthalmol 1988;106:337–40.

9.) Vitamin supplement use and incident cataracts in a population-based study. Arch Ophthalmol 2000;118:1556–63.

10.) Antioxidant vitamins and nuclear opacities. The Longitudinal Study of Cataract. Ophthalmology 1998;105:831–6.

11.) Long-term supplementation with alpha-tocopherol and beta-carotene and age-related cataract. Acta Ophthalmol Scand 1997;75:634–40.

12.) Long-term vitamin C supplement use and prevalence of early age-related lens opacities. Am J Clin Nutr 1997;66:911–6.

13.) Nutrient intake and cataract extraction in women: a prospective study. BMJ 1992;305:335–9.

14.) A prospective study of carotenoid and vitamin A intakes and risk of cataract extraction in US women. Am J Clin Nutr 1999;70:509–16.

15.) Lutein, but not alpha-tocopherol, supplementation improves visual function in patients with age-related cataracts: a 2-y double-blind, placebo-controlled pilot study. Nutrition 2003;19:21–4.

16.) Rejuvenation of visual functions in older adult drivers and drivers with cataract during a short-term administration of N-acetylcarnosine lubricant eye drops. Rejuvenation Res. 2004 Fall;7(3):186-98.

17.) Efficacy of N-acetylcarnosine in the treatment of cataracts.Drugs R D. 2002;3(2):87-103.

18.) The effect of a topical antioxidant formulation including N-acetyl carnosine on canine cataract: a preliminary study.Vet Ophthalmol. 2006 Sep-Oct;9(5):311-6

19.) N-Acetylcarnosine, a natural histidine-containing dipeptide, as a potent ophthalmic drug in treatment of human cataracts.  Peptides. 2001 Jun;22(6):979-94

Cellulite

Natural Strategies For Fighting Cellulite

The only people who “don’t believe in cellulite” are people — mostly men — who don’t have any!

Cellulite isn’t “just fat” – it is fat that has undergone a “mattress effect” due to the underlying landscape of connective tissue. It occurs far more frequently in women than in men and is influences by female hormones. When seen in men, cellulite suggests a possible androgen (male hormone) deficiency or estrogen excess.

Cellulite is not due only to overweight, since normal weight people can have cellulite and many fat people do not. However, excess weight amplifies the appearance of cellulite in most cellulite-prone people.

Cellulite is thought to be a “multi-factorial” condition. Factors that contribute to the development of cellulite include:

  • Female hormones, especially estrogen
  • Collagen fiber break-down (as occurs with age and nutrient deficiencies)
  • Poor venous and lymphatic circulation
  • Overweight

Although believed by many to be largely a cosmetic problem, cellulite tissue often feels heavy or tight and is often tender when massaged. (NOTE: DO NOT confuse this with “cellulitis,” a serious inflammation or infection of connective tissue. There is no underlying infection in cellulite).

Books and tabloid articles have been written about “cellulite cures” and diet changes, although there is little substantiation for this in the medical literature
apart from overall weight loss.

Diet And Lifestyle Recommendations

  • Maintain a normal weight. Excess body fat alone does not cause cellulite, but it does increase estrogen levels. Excess body fat typically makes
    cellulite more noticeable. For weight loss help, try The Super Fast Diet.
  • Exercise: regular aerobic exercise with weight training for specific problem areas may be helpful. Exercise is known to improve estrogen balance and assist with weight (fat) loss. Spot exercises for lifting the glutes (butt) and hips may help reduce the appearance of cellulite on thighs.
  • Massage: daily self-massage of cellulite tissue, using the hands with a “kneading” motion. Massage helps break up the problematic connective tissue and improve venous and lymphatic circulation. Special percussion massage therapy may be particularly helpful.

Primary Support

  • Maxi Multi: 3 caps, 3 times per day with meals. Optimal (not minimal) doses of antioxidants & bioflavonoids are particularly important for strengthening blood vessels, reducing inflammation and decreasing free radicals. Vitamin C is crucial to collagen formation.

Additional Support (Internal)

  • Maxi Flavones:1 cap, 1-2 times per day with meals. High potency antioxidant / flavonoid herbs to strengthen blood vessels, decrease inflammation and improve liver function (which in turn helps hormone balance).
  • Conjugated Linoleic Acid (CLA): 4-5 caps per day with meals. CLA has been shown to decrease body fat, increase lean muscle tissue   and assist  with cellulite improvement.
  • Gotu kola (Centella asiatica): 1 cap, 3 times per day with meals. (Target dose: 90 mg triterpenes per day)
  • Horse chestnut (Aesculus hippocastanum): 1 cap, 3 times per day with meals. (Target dose:30- 60mg escin per day).

Additional Support (Topical)

Topical preparations containing caffeine, xanthines and related thermogenic substances, and glycyrrhetinic acid (from licorice) may have benefit.

Tests

Males with cellulite should have a male hormone profile test performed. When seen in men, cellulite is highly suggestive of a male hormone deficiency and/or an excess of estrogens.

References

1.) Querleux B, Cornillon C, Jolivet O, Bittoun J. Anatomy and physiology of subcutaneous adipose tissue by in vivo magnetic resonance imaging and spectroscopy: relationships with sex and
presence of cellulite.
Skin Res Technol. 2002 May;8(2):118-24.
2.) Rosenbaum M, Prieto V, Hellmer J, Boschmann M, Krueger J, Leibel RL, Ship AG. An exploratory investigation of the morphology and biochemistry of cellulite. Plast Reconstr Surg.
1998 Jun;101(7):1934-9.
3.) Piérard GE, Nizet JL, Piérard-Franchimont C. Cellulite: from standing fat herniation to hypodermal stretch marks. Am J Dermatopathol. 2000 Feb;22(1):34-7.
4.) Mirrashed F, Sharp JC, Krause V, Morgan J, Tomanek B. Pilot study of dermal and subcutaneous fat structures by MRI in individuals who differ in gender, BMI, and cellulite grading. Skin Res Technol. 2004 Aug;10(3):161-8.
5.) Pavicic T, Borelli C, Korting HC. Cellulite–the greatest skin problem in healthy people? An approach. J Dtsch Dermatol Ges. 2006 Oct;4(10):861-70.
6.) Quatresooz P, Xhauflaire-Uhoda E, Piérard-Franchimont C, Piérard GE. Cellulite histopathology and related mechanobiology. Int J Cosmet Sci. 2006 Jun;28(3):207-10.
7.) Piérard GE. Commentary on cellulite: skin mechanobiology and the waist-to-hip ratio.J Cosmet Dermatol. 2005 Sep;4(3):151-2.
8.) Rotunda AM, Avram MM, Avram AS.Cellulite: Is there a role for injectables? J Cosmet Laser Ther. 2005 Dec;7(3-4):147-54.
9.) A. V. Rawlings. Cellulite and its treatment. Int J. of Cosmetic Science. 2006 Feb; 28(3):175-190.
10.) Velasco M.V.,Tano C.T.,Machado-Santelli G., Consiglieri V.O., et al. Effects of caffeine and siloxanetriol alginate caffeine, as anticellulite agents, on fatty tissue: histological evaluation.
J. Cosmetic Derm. 2008 Jan; 7(1):23-29.
11.) Lupi O., Semenovitch I., Treu C., Bottino D., Bouskela E. Evaluation of the effects of caffeine in the microcirculation and edema on thighs and buttocks using the orthogonal polarization
spectral imaging and clinical parameters.
J. Cosmetic Derm. 2007 May; 6(2): 102-107.
12.) Smalls LK, Hicks M, Passeretti D, Gersin K, Kitzmiller WJ, Bakhsh A, Wickett RR, Whitestone J, Visscher MO. Effect of weight loss on cellulite: gynoid lypodystrophy.Plast Reconstr Surg. 2006
Aug;118(2):510-6.
13.) Distante F, Bacci PA, Carrera M. Efficacy of a multifunctional plant complex in the treatment of the so-called ‘cellulite’: clinical and instrumental evaluation. Int J Cosmet Sci. 2006 Jun;28(3):191-206.
14.) Rona C, Carrera M, Berardesca E.Testing anticellulite products.Int J Cosmet Sci. 2006 Jun;28(3):169-73.
15.) Armanini D, Nacamulli D, Francini-Pesenti F, Battagin G, Ragazzi E, Fiore C. Glycyrrhetinic acid, the active principle of licorice, can reduce the thickness of subcutaneous thigh fat through topical application. Steroids. 2005 Jul;70(8):538-42.

Children’s Basic Nutrients

Kids Need Great Supplements Too!

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

Dosage: 1 to 2 capsules three times daily.

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

Dr. Myatt’s Cardiovascular Risk Checklist

A Medical White Paper Presented By Dr. Dana Myatt

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

Shocking Facts about Heart Attacks

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

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

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

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

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

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

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

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

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

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

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

Good News About “Emerging Risk Factors”

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

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

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

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

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

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

Name: Email:

We respect your email privacy

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

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

Dr. Myatt’s Cardiovascular Risk Checklist Lab Tests

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

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

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

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

Sorry – Currently unavailable – please check back soon!

Castor Oil Packs

How to use this effective detoxifying treatment

Materials Needed

  • Wool flannel – un-dyed, un-treated, un-bleached
  • Cold pressed castor oil
  • Electric heating pad
  • Baking dish
  • Plastic sheet (or 2 plastic trash bags, large size)
  • Old bath towel

Instructions for Use

Place the wool flannel in a baking dish. (Use any suitable baking dish for a conventional oven; use a glass baking dish for the microwave oven). The cloth should be folded at least 3 thicknesses for use. Pour castor oil over the flannel, sufficient to saturate it through all thicknesses. Get the pack wet with castor oil but not dripping. Place the baking dish in the oven, microwave oven, or hot plate until it is quite warm. Be careful not to burn the pack or to get it so hot that it will burn you.

Spread the plastic sheet or bags on the bed, couch, or where ever you will be using the pack. Place the bath towel on top of the plastic. Plug in the heating pad.

After the pack is warm (again, be careful not to burn yourself!!), apply it to the indicated area. Put the heating pad on top of the pack and leave it in place for at least one hour, or as recommended.

You may want to put an additional piece of plastic over the top of the pack to prevent the oil from staining bed, couch, or chair. The reason for the use of the plastic is to protect fabrics.

When you are finished using the pack, put it back in the baking dish and leave it for next time. You DO NOT wash the pack between uses. If the pack begins to dry out, simply add more castor oil the next time you use it.

Also when you are finished, clean the skin with 2 teaspoons of baking soda added to a quart of water. The pack draws toxins out of the body and these can be reabsorbed or cause a skin rash if not removed by cleaning the skin.

It is best to do some relaxing or meditative exercise while you are using the pack. This is a good time to practice visualization exercises, listen to personal-growth audio or video tapes, or meditate. It is also fine to sleep with the pack in place, but be sure to remove the heating pad when sleeping to avoid burning the skin.

Children’s Health

Raise Healthier Children Naturally

Healthy, Happy Children - Naturally!Children aren’t just “little adults.” Because their bodies are in “fast growth mode,” they have different nutritional requirements than adults.

Because still-growing bodies soak up nutrients like sponges, diet and nutrient deficiencies will have a bigger and more noticeable impact on a child than on an adult. In other words, good nutrition is even more important in childhood and young adulthood that at any other time of life. The nutrition your child receives today will impact him or her for the rest of their life.

While conventional medicine is sometimes necessary to treat certain childhood illnesses, most problems can be better managed through natural means. Less negative side-effects and a true “correction” of underlying problems (instead of just a “band aid” approach) are among the reasons many parents choose natural alternatives over synthetic options.

Children can use many of the “adult” remedies, especially herbs. Here is a convenient equation for adjusting an herb or nutrient dose for a child based on body weight.

Child-Friendly Supplements Health Concerns
of Children
Children’s Vitamins
Greens Firse Berry / Red Alert
Similase Jr.

Whey Protein ADD/ADHD
Allergies
Asthma
Attention Deficit
Colds and Flu
Diarrhea
Diarrhea
Parasites

Coconut Oil (Organic, Virgin)

This Oil Should Be in Your Kitchen AND Your Medicine Cabinet

Coconut Oil - A Healthy Oil Of Many UsesCoconut oil is a saturated fat, which means it doesn’t go rancid when heated or when stored for long periods of time.

Essential Fatty Acids (EFA’s) turn into unhealthy “trans fats” when heated, so although you need EFA’s for good health, you should NOT cook with them! Even olive oil, a polyunsaturated fat (PUFA)  should NOT be used for cooking. (Olive oil is NOT an essential fat).

Coconut oil and other saturated fats are heat-stable. For frying and deep-frying, coconut oil is one of the very best oils to use.

In addition to being heat-stable and great for cooking, coconut oil has the following health advantages:

  • Coconut oil contains lauric acid and other a medium-chain triglycerides (MCT’s) with powerful antimicrobial effects against a wide range of bacteria, viruses, fungi / yeasts and protozoa. (1-7)
  • The MCT’s in coconut oil activate the immune system. (8,9)
  • Coconut oil’s MCT’s have proven anti-tumor effects. (10,11)
  • MCT’s in coconut oil aid weight loss three ways: by decreasing hunger, increasing fat-burning and increasing metabolism. (12-19)
  • Lowers cholesterol and improves blood fat levels. (20-22)

If you’ve heard bad things about saturated fats, you should know that it’s all nonsense – bogus B.S. promoted by the soy oil industry and Big Business. (Can you say “Proctor and Gamble”?) Read about the unjustified “bad press” that this miraculous oil has suffered here: Saturated Fat: Another Big, Fat Lie

We offer organic, virgin coconut oil, the finest quality available. Use coconut to cook, make pie crusts or anything that calls for “Crisco” (Crystallized Cottonseed Oil, a product not fit for human consumption).

Use Coconut Oil, two to four tablespoons per day as a food, substituted for whatever oils you currently cook with (except butter which is a true health food). Heck, you can even use coconut oil on your skin as a moisturizer, protectant and anti-microbial!

Coconut Oil (Organic, Virgin) 15 fl. ounces   $15.95

Please Note: Coconut oil is slippery stuff – and it may seep from it’s container during shipment. We have received reports of coconut oil seeping out of still-tightly-sealed jars! We double-bag this product and pack it carefully for shipping but we cannot be responsible for leakage during shipment – there will be no returns or refunds on this product.

References

1.) Antimicrobial activity of potassium hydroxide and lauric acid against microorganisms associated with poultry processing. J Food Prot. 2006 Jul;69(7):1611-5.
2.) In vitro activity of lauric acid or myristylamine in combination with six antimicrobial agents against methicillin-resistant Staphylococcus aureus (MRSA). Int J Antimicrob Agents. 2006 Jan;27(1):51-7. Epub 2005 Nov 28.
3.) Susceptibility of Clostridium perfringens to C-C fatty acids.Lett Appl Microbiol. 2005;41(1):77-81.
4.) Effect of lauric acid and nisin-impregnated soy-based films on the growth of Listeria monocytogenes on turkey bologna. Poult Sci. 2002 May;81(5):721-6.
5.) Inhibition of bacterial foodborne pathogens by the lactoperoxidase system in combination with monolaurin. Int J Food Microbiol. 2002 Feb 25;73(1):1-9.
6.) Fatty acids and derivatives as antimicrobial agents. Antimicrob Agents Chemother. 1972 Jul;2(1):23-8.
7.) Susceptibility of Helicobacter pylori to bactericidal properties of medium-chain monoglycerides and free fatty acids. Antimicrob Agents Chemother. 1996 Feb;40(2):302-6.
8.) Saturated triglycerides and fatty acids activate neutrophils depending on carbon chain-length. Eur J Clin Invest. 2002 Apr;32(4):285-9.
9.) Immunonutrition–supplementary amino acids and fatty acids ameliorate immune deficiency in critically ill patients. Langenbecks Arch Surg. 2001 Aug;386(5):369-76.
10.) Antitumor effect of medium-chain triglyceride and its influence on the self-defense system of the body. Cancer Detect Prev. 1998;22(3):219-24.
11.) Effects of calcitriol, seocalcitol, and medium-chain triglyceride on a canine transitional cell carcinoma cell line. Anticancer Res. 2005 Jul-Aug;25(4):2689-96.
12.) Value of VLCD supplementation with medium chain triglycerides.Int J Obes Relat Metab Disord. 2001 Sep;25(9):1393-400.
13.) The thermic effect is greater for structured medium- and long-chain triacylglycerols versus long-chain triacylglycerols in healthy young women. Metabolism. 2001 Jan;50(1):125-30.
14.) Greater rise in fat oxidation with medium-chain triglyceride consumption relative to long-chain triglyceride is associated with lower initial body weight and greater loss of subcutaneous adipose tissue. Int J Obes Relat Metab Disord. 2003 Dec;27(12):1565-71.
15.) Thermogenesis in humans during overfeeding with medium-chain triglycerides.Metabolism. 1989 Jul;38(7):641-8.
16.) Dietary medium-chain triacylglycerols suppress accumulation of body fat in a double-blind, controlled trial in healthy men and women.J Nutr. 2001 Nov;131(11):2853-9.
17.) Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride. Am J Clin Nutr. 1982 Apr;35(4):678-82.
18.) Medium-chain triglycerides increase energy expenditure and decrease adiposity in overweight men.Obes Res. 2003 Mar;11(3):395-402.
19.) Comparison of diet-induced thermogenesis of foods containing medium- versus long-chain triacylglycerols.J Nutr Sci Vitaminol (Tokyo). 2002 Dec;48(6):536-40.
20.) Effect of dietary medium- and long-chain triacylglycerols (MLCT) on accumulation of body fat in healthy humans. Asia Pac J Clin Nutr. 2003;12(2):151-60.
21.) Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation. Clin Biochem. 2004 Sep;37(9):830-5.
22.) Effect of medium-chain triglycerides on the postprandial triglyceride concentration in healthy men. Biosci Biotechnol Biochem. 2003 Jan;67(1):46-53.