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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

1.) Freedland SJ, Mavropoulos J, Wang A, Darshan M, Demark-Wahnefried W, Aronson WJ, Cohen P, Hwang D, Peterson B, Fields T, Pizzo SV, Isaacs WB. Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. Prostate. 2008 Jan 1;68(1):11-9.
2.) Venkateswaran V, Haddad AQ, Fleshner NE, Fan R, Sugar LM, Nam R, Klotz LH, Pollak M. Association of diet-induced hyperinsulinemia with accelerated growth of prostate cancer (LNCaP) xenografts.J Natl Cancer Inst. 2007 Dec 5;99(23):1793-800. Epub 2007 Nov 27.
3.) Zhou W, Mukherjee P, Kiebish MA, Markis WT, Mantis JG, Seyfried TN. The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer.Nutr Metab (Lond). 2007 Feb 21;4:5.
4.) Borugian MJ, Sheps SB, Kim-Sing C, Van Patten C, Potter JD, Dunn B, Gallagher RP, Hislop TG. Insulin, macronutrient intake, and physical activity: are potential indicators of insulin resistance associated with mortality from breast cancer? Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1163-72.
5.) Seyfried TN, Sanderson TM, El-Abbadi MM, McGowan R, Mukherjee P.: Role of glucose and ketone bodies in the metabolic control of experimental brain cancer.Br J Cancer. 2003 Oct 6;89(7):1375-82.
6.) Muti P, Quattrin T, Grant BJ, Krogh V, Micheli A, Schünemann HJ, Ram M, Freudenheim JL, Sieri S, Trevisan M, Berrino F. Fasting glucose is a risk factor for breast cancer: a prospective study. Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1361-8.
7.) Meixensberger J, Herting B, Roggendorf W, Reichmann H: Metabolic patterns in malignant gliomas.J Neurooncol 1995, 24:153-161
8.) Fearon KC.: Nutritional pharmacology in the treatment of neoplastic disease.Baillieres Clin Gastroenterol. 1988 Oct;2(4):941-9.
9.) Pedersen PL: Tumor mitochondria and the bioenergetics of cancer cells. Prog Exp Tumor Res 1978, 22:190-274.

Garlic

1.) Morioka, N., Morton, D.L., and Irie, R.F.: A protein fraction from aged garlic extract enhances cytotoxicity and proliferation of human lymphocytes mediated by interleukin-2 and conavalin. Proc Ann Meet Am Assoc Cancer 34:A3297, 1993.
2.) Legnani C., Frascaro M., Guazzaloca G., et al.: Effects of a dried garlic preparation on fibrinolysis and platelet aggragation in healthy subjects. Arzneim Forsch Drug Res 43:119-122, 1993.
3.) Kiesewetter H., et al.: effects of garlic coated tablets in peripheral arterial occlusive disease. Clin Investig 71:383-86, 1993.
4.) Lau, B.H., Yamasaki, T., and Gridley, D.S.: Garlic compounds modulate macrophage and T-lymphocyte function. Mol Biother 3:103-107, 1991.
5.) Dausch JG., Nixon DW.: Garlic: a review of its relationship to malignant disease. Prev Med 19:346-61, 1990.
6.) Kandil O.M., et al.: Garlic and the immune system in humans: its effect on natural killer cells. Fed Proc 46:441, 1987.
7.) Kandil, O.M. et. al.: Garlic and the immune system in humans: Its effect on natural killer cells. Fed Proc 46:441, 1987.
8.) Belman S.: Onion and garlic oils prohibit tumor promotion. Carcinogenesis 4(8):1063-5, 1983.
9.) Kroning, F.: Garlic as an inhibitor for spontaneous tumors in predisposed mice. Acta Unio Inter Contra Cancrum 20(3):855, 1964.

Super Foods

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

Exercise and Cancer

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

Support Groups

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

Stop Tobacco and Alcohol Use

1.) Kaufman EL, Jacobson JS, Hershman DL, Desai M, Neugut AI. Effect of breast cancer radiotherapy and cigarette smoking on risk of second primary lung cancer. J Clin Oncol. 2008 Jan 20;26(3):392-8.
2.) Park SM, Lim MK, Jung KW, Shin SA, Yoo KY, Yun YH, Huh BY. Prediagnosis smoking, obesity, insulin resistance, and second primary cancer risk in male cancer survivors: National Health Insurance Corporation Study. J Clin Oncol. 2007 Oct 20;25(30):4835-43.
3.) Koskinen WJ, Brøndbo K, Mellin Dahlstrand H, Luostarinen T, Hakulinen T, Leivo I, Molijn A, Quint WG, Røysland T, Munck-Wikland E, Mäkitie AA, Pyykkö I, Dillner J, Vaheri A,
Aaltonen LM. Alcohol, smoking and human papillomavirus in laryngeal carcinoma: a Nordic prospective multicenter study. J Cancer Res Clin Oncol. 2007 Sep;133(9):673-8. Epub 2007 May 8.
4.) Muwonge R, Ramadas K, Sankila R, Thara S, Thomas G, Vinoda J, Sankaranarayanan R. Role of tobacco smoking, chewing and alcohol drinking in the risk of oral cancer in Trivandrum, India: A nested case-control design using incident cancer cases. Oral Oncol. 2007 Oct 12
5.) Chen CH, Shun CT, Huang KH, Huang CY, Tsai YC, Yu HJ, Pu YS. Stopping smoking might reduce tumour recurrence in nonmuscle-invasive bladder cancer. BJU Int. 2007 Aug;100(2):281-6; discussion 286. Epub 2007 Apr 5.
6.) Rieck G, Fiander A.The effect of lifestyle factors on gynaecological cancer. Best Pract Res Clin Obstet Gynaecol. 2006 Apr;20(2):227-51.
7.) Ford MB, Sigurdson AJ, Petrulis ES, Ng CS, Kemp B, Cooksley C, McNeese M, Selwyn BJ, Spitz MR, Bondy ML.Effects of smoking and radiotherapy on lung carcinoma in breast carcinoma
survivors. Cancer. 2003 Oct 1;98(7):1457-64.
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.
Curr Opin Urol. 2003 Mar;13(2):147-51.
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
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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
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Vitamin D

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

Bromelain (anasas comosus)

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

 

Senior Health


Good Health for the Golden Years

Healthy, Active SeniorsAs I wrote in one HealthBeat article, “The ‘golden years’ can kiss my grits.” What I meant was that “The Golden Years” — that time in life when the family is raised and we are “hopefully” financially secure enough to stop working full time, and to travel or work at our favorite hobbies if we so choose — are often tarnished by failing health. I think that’s a pity, but it doesn’t have to be that way.

If you read the discussion on aging at the Anti-Aging Health Solution Center, you know that the human life expectancy should be on the order of 120 years. I’m not talking about just living long, either. I’m talking about spending those years in good health. Many people start crawling toward the grave from young or middle adulthood, plagued with aches, pains and illnesses. That’s not the way it is in many cultures.

By following some Basic Rules of Good Health and choosing natural, corrective measures over often-dangerous drugs and surgical “band aids,” a longer, healthier life is certainly possible.

Please visit these various areas of our site to find out how to be healthy and happy well into old age.

The Health Solutions Center at Left is a Great Place to Begin Your Search for Better Health.

Here are some additional articles for past HealthBeat News that you may find of benefit:

Neurological Disease: What You’re NOT Going to Hear From Your Conventional Doctor

Rejuvenate Your Heart in 9 Simple Steps

5 Proven Ways to Slow Dementia and Alzheimer’s

7 Ways to Decrease Your Cancer Risk

Stay informed! Claim your own  FREE subscription to HealthBeat News here: HealthBeat News

 

PSA CAPSULES (formerly called Prostate Support)


A PC-SPES-Like Herbal Formula for Prostate Cancer

Prostate Support – now called PSA Capsules – contains a combination of herbs that support the prostate gland and immune system in the presence of prostate cancer. This formula is similar to “PC-SPES” without the undisclosed drugs.

Suggested dose: 1-2 capsules, 3 times per day on an empty stomach.

Dr. Myatt’s comment: It is important to work with a skilled holistic physician when treating any form of cancer.

Each (two) capsules contain:
(Please Note: Due to variances in the processing of these herbs, actual mg amounts may vary slightly)

Reishi mushroom (Ganoderma lucidum)………..172 mg
Baikal skullcap root (Scutellaria baicalensis)…..146 mg
Rabdosia root (Rabdosia rubescens) …………….120 mg
San-Qi ginseng root (Panax notoginseng)……….112 mg
Ban Lan Gen root (AKA Dyer’s Woad root)
(Isatis indigotica)…………………………………………………94 mg
Mum flower (Dendranthema morifolium) …………..78 mg
Saw Palmetto berry (Serenoa repens)……………….70 mg
Licorice root (Glycyrrhiza glabra)…………………………70 mg

NOTE: This product is only available to Dr. Myatt’s private practice patients.

The Truth about PC-SPES

The product PC SPES worked well for many men. Unfortunately, it contained a number of undisclosed drugs which not only caused some undesirable side effects such as breast enlargement and tenderness, but also side effects that could be downright dangerous, even lethal. When tested, PC-SPES was found to contain diethylstilbesterol (DES), a synthetic form of the female hormone estrogen. This compound can cause a number of negative side effects, the most significant of which is blood clotting which can lead to cardiovascular events including heart attach and stroke, deep vein thrombosis (DVT) and pulmonary embolism (PE).

Another compound found in PC-SPES was Warfarin (aka “rat poison”) – a powerful blood thinner presumably included to counter the potential blood clotting effects of the DES. Finally, the drug Indomethacin (Indocid) – a non-steroidal anti-inflammatory (NSAID)- was found. This drug has the potential to cause severe gastrointestinal side effects such as GI bleeding, ulceration and blood clotting problems.

It is believed that the great success of PC Spes was due to the undisclosed DES (female hormone). As many have noted, men would vary the dose to achieve the best  effect – from one or two to as many as a dozen capsules per day. This exposed men to potentially very dangerous levels of the other undisclosed drugs in addition to high hormone levels.

I am including a link to a very informative paper on this subject, an essay by Subhuti Dharmananda, Ph.D., Director, Institute for Traditional Medicine, Portland, Oregon

ITM Online

Dr. Myatt’s product Prostate Support is the result of Dr. Myatt’s suspicions about the product PC Spes and her analysis of it which demonstrated the undisclosed drugs. She then formulated a replacement which contained the beneficial herbal components, without the potentially dangerous drugs. The drugs that were hidden in PC Spes are all easily available to a physician if they are needed, and Dr. Myatt felt that it was far safer and more effective to use carefully tailored separate doses of these drugs when necessary to achieve the desired effects.

This allowed Dr. Myatt to develop a very effective herbal formulation, without risking the potentially dangerous, even lethal side effects that could result from the hidden drugs. Her further observation regarding the PC Spes formula was that if the manufacturer was willing to hide drugs in it’s formula, what else was it willing to do? The drug were undisclosed – this means that the doses were also undisclosed and could be changed or even eliminated at any time.

As you will have seen from this website, we at The Wellness Club have no love for the FDA. In this instance, however, we believe that they did the right thing by removing PC Spes from the marketplace.

Dr. Myatt has a great deal of experience in treating prostate cancer. She also has a very personal interest – she has been treating her own father for prostate cancer for the two decades. His conventional physicians wanted to do the  “cut, burn, and poison” treatments when it was first discovered. Instead, Dr. Myatt pioneered a then-unconventional form of hormonal suppression therapy. This proved highly successful and she has used these techniques on hundreds of men since then with the same excellent results. Her techniques are now accepted and commonly used in conventional medicine.

Please visit our web pages where we discuss Cancer , Prostate Cancer , Prostate Enlargement , and Man Health & Fitness where Dr. Myatt discusses male hormones. There is information available on hormone testing on our Medical Tests page.

As I mentioned, my recommendation to any man who is dealing with prostate cancer – at any stage of development or treatment – is to run, not walk, to arrange a consultation with Dr. Myatt! Please see the information regarding her alternative medicine consultations  – a consultation with Dr. Myatt is an excellent investment in good health, and her patients find that the cost of her consultations is more than offset by the improved health and the money saved on both prescription drugs and treatments and on other non-prescription “treatments” of questionable value and safety.

Although different in every man who has it, prostate cancer is almost always a disease that can be managed as a chronic condition (like diabetes). Prostate cancer should certainly not be a death sentence when treated appropriately.

A transcript of the original, fully annotated notes for a lecture on Prostate Cancer presented by Dr. Myatt in May of 2000 at the 2000 Pacific Northwest Herbal Symposium may be found at the link below: Botanical and Nutritional Considerations in the Treatment of Prostate Cancer –
Dana Myatt, N.M.D.

 

Female Hormone Profile (Pre-Menopausal)

FEMALE HORMONE PROFILE (PRE-MENOPAUSAL)

This panel uses saliva samples to measure free estradiol, progesterone, DHEA, testosterone, FHS and LH in pre-menopausal females, following hormone levels throughout the monthly cycle. The test requires 11 saliva samples taken over one complete female cycle.

Dr. Myatt’s comment: Useful in discovering hormone imbalances related to infertility, PMS, irregular cycles, polycystic ovary disease, endometriosis, fibroids and to determine overall sex hormone levels consistent with peri-menopause.

Click here to download an informational brochure on the Pre-menopausal Female Hormone Profile

FEMALE HORMONE PROFILE (PRE-MENOPAUSAL) #989 $479.00

(Sorry – not available in New York state)

 

Fertility Restore Female Hormone Profile

FEMALE HORMONE PROFILE (POST-MENOPAUSAL)

This panel uses saliva samples to measure estriol, estrone, estradiol, progesterone, DHEA, DHEA-S and testosterone in post-menopausal females.

A female hormone profile is especially valuable in post-menopausal hormone (or herbal) replacement therapy because it allows the doctor to make a “custom-tailored” prescription instead of a “generic” one.

Please NOTE: this test is best used by a woman who has NOT yet been on hormone replacement therapy, not as a follow-up to therapy. The Comp. Plus Hormone Profile is much more accurate and provides “preventive” information like the 2/16 ratio for breast cancer prevention which this saliva test does not. I highly recommend the Comp Plus Profile over the saliva testing. I will no longer renew hormone prescriptions on the basis of a saliva test. — Dr. Myatt

FEMALE HORMONE PROFILE POST-MENOPAUSAL #991 $154.00

(Sorry – not available in New York state)


FEMALE HORMONE PROFILE (PRE-MENOPAUSAL)

This panel uses saliva samples to measure free estradiol, progesterone, DHEA, testosterone, FHS and LH in pre-menopausal females, following hormone levels throughout the monthly cycle. The test requires 11 saliva samples taken over one complete female cycle.

Dr. Myatt’s comment: Useful in discovering hormone imbalances related to infertility, PMS, irregular cycles, polycystic ovary disease, endometriosis, fibroids and to determine overall sex hormone levels consistent with peri-menopause.

Click here to download an informational brochure on the Pre-menopausal Female Hormone Profile

FEMALE HORMONE PROFILE (PRE-MENOPAUSAL) #989 $479.00

(Sorry – not available in New York state)

 

Anti-aging and Longevity:

The Science of Aging Well

Every living species appears to have a genetically-programmed maximum lifespan. Scientists and geneticists believe that the human lifespan should be around 120 years. For as technologically advanced as modern medicine is, one wonders why we still have so many “incurable” diseases and why the average life expectancy in the US is still only 70 years. (According to the World Health Organization, The United States rated 24th in the world for life expectancy; an average of 70.0 years of healthy life for babies born in 1999).

This means that most people aren’t even reaching 2/3 of their life expectancy! And for many, even a significant number of those “70-ish years” are spent in poor health and decreased capabilities.

A lot more is known about slowing the aging process than you’ll ever hear from conventional medicine. Remember, conventional medicine is in business to sell drugs and surgery to “band aid” disease, not prevent disease, cure disease (especially chronic disease) or slow the aging process.

There are many life-extending scientific findings that never find their way into mainstream medicine. The following are some of the most well-researched anti-aging and longevity measures you can take to slow the aging process and enjoy more years of good health.

Top Anti-Aging Supplements and Herbs

Anti-Aging Therapies
Table of Contents

Age-Related Health Concerns
by Topic

Multiple Vitamin/Mineral Formula Age-Related Memory Changes CoQ10 Age-Related Vision Loss Acetyl L-Carnitine Atherosclerosis Alpha Lipoic Acid Arthritis-Osteoarthritis Vitamin D Arthritis-Rheumatoid DHEA Blood Pressure – High Melatonin Cancer Prevention Male hormones Cancer Treatment Female hormones Hair Loss Ginkgo Menopause, Female Vinpocetin Menopause, Male (Andropause) Glucosamine sulfate Neurological Disease Grape Seed Extract Osteoporosis Other Anti-Aging Supplements Prostate Cancer Prostate Enlargement Stroke

Multi Vitamin/Mineral Formula – Not a “once per day” pill (they don’t contain enough of anything to have any effect except preventing severe deficiency disease). A complete anti-aging multiple should include optimal doses of antioxidants like vitamin C, E and carotenes, B complex vitamins, minerals such as zinc, selenium, calcium and magnesium. Here is a list of the optimal daily doses of vitamins, minerals and trace minerals that should be included in your daily anti-aging multiple vitamin.

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

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

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

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

Alpha Lipoic Acid, a Neurological Antioxidant and Energy Transporter, improves mitochondrial function (the “energy producing units” of the cell) and works well in combination with CoQ10 and Acetyl-l-Carnitine to enhance energy production. A decrease of mitochondrial function is believed by many researchers to be one of the primary causes of aging. Lipoic acid is also involved in the conversion of carbohydrates to energy

Vitamin D increases calcium absorption. Deficiencies of Vitamin D are associated with osteoporosis, rheumatic pains, and dental disease. Higher intakes of vitamin D have been shown to protect the body from cancer, especially prostate and breast cancer. Many authorities are recommending that the recommended adult daily dose should be raised from 400 IU to 1,000 IU. Doses of 1,000-2,000 are not only safe, they may be needed for disease prevention.

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

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

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

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

Male hormones: testing and replacement

Female hormones: testing and replacement

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

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

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

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

Grape Seed Extract (OPC’s) is an antioxidant that exhibits 50 times more antioxidant power than vitamin E and 20 times more than vitamin C. OPC’s from Grape Seed Extract easily cross the blood-brain barrier and prevent free radical damage to the brain and nervous system. Grape seed extract also improves blood viscosity (the same “magic” as red wine but without the calories, carbs or liver toxicity).

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

Other Anti-Aging supplements include lutein, SAMe, fish oil, green tea extract, and COX-2 Support. Maintenance of a normal body weight is the single most important dietary/lifestyle measure associated with longevity and good health.

To learn more about specific protocols for age-related topics, please visit specific health concerns here:

Age-Related Cognitive Decline (Dementia, Alzheimer’s, Senility)

Age-Related Vision Loss (Cataracts, Macular Degeneration, Glaucoma)

Atherosclerosis

Arthritis-Osteoarthritis

Arthritis-Rheumatoid

Blood Pressure – High

Cancer Prevention and Cancer Treatment

Male Pattern Baldness

Menopause, Female

Menopause, Male (Also called “Andropause”)

Neurological Disease (ALS, MS, Parkinson’s)

Osteoporosis

Prostate Cancer

Prostate Enlargement

Stroke

Back Pain

Natural Support For This Common And Troublesome Condition

Back pain is second only to headache as the most common presenting complaint to a family practice physician. If the back pain is sudden in onset, persists for more than two weeks, or results in loss of bowel or bladder control, see a physician immediately. A herniated disc can cause such pain. (Although most “sudden onset” back complaints are due only to muscle stress).

Most back pain is due to mild deterioration of the bones in the lower back, loss of joint material, simple dehydration, arthritis, mineral imbalances, weak muscle tone, and high stress levels. Most cases of low back pain can be cured through self-help measures.

Diet And Lifestyle Recommendations

  • Drink a minimum of 64 ounces of pure water daily. Simple dehydration can cause disc material to weaken.
  • Maintain a normal weight. Excess weight places a great stress on the lumbar spine.
  • Low back and abdominal exercises help stretch and strengthen supporting structures. (See below). These take less than 10 minutes per day but are priceless for correcting low back pain.
  • A diet high in vegetables and/or fruits helps strengthen supporting ligaments and tendons. Add one tablespoon of gelatin per day to your daily diet.
  • Practice stress reduction techniques such as meditation. Stress is now known to be a major factor in the development and maintenance of low back pain by causing abnormal muscle tension.

Primary Support

  • Maxi Multi: 3 caps, 3 times per day with meals. Optimal doses (not minimal doses) of Vitamins C, E, zinc, selenium, calcium, magnesium, boron and bioflavonoids are especially important.
  • Bromelain: 2 caps, 3-4 times per day between meals. Bromelain acts as a natural anti-inflammatory agent.

Additional Support

For arthritis or degenerative disc disease:

  • Glucosamine Sulfate (Pharmaceutical grade): 2 caps (750mg each), 2 times per day for 4 weeks, then 1 cap, 2 times per day thereafter. (Target dose: 3,000mg for 4 weeks, then 1,500 per day thereafter).
  • MSM (Fundamental sulphur): 1,000mg, 3 times per day with meals.
  • Cal-Mag: 1 cap, 3 times per day with meals in addition to the 1,000:500mg contained in Maxi Multi. If you are using another multiple formula, make sure to get 1,200-1,500mg of calcium and 500-750mg of magnesium daily total.
  • COX-2-Support: a powerful combination of anti-inflammatory herbs. Can be used in addition to bromelain for extra pain relief.

Low Back Exercises

1.) Pelvic tilt. Tilt small of back toward floor. Tighten butt muscles and lift hips. Hold for count of 10. Repeat 5-20 times.

2.) Knee pull-ups. Pull knee to forehead with both hands. Raise head off floor to meet knee. Return slowly to start. Alternate sides. Repeat 5-10.

3.) Low back stretch. Bring one knee as close to chest as possible. Return to start. Alternate sides. Repeat 5-10 times each side.

4.) Curl-ups. Raise trunk toward bent knees. Hold for 10 seconds. return to start. Repeat 5-20 times.

5.) Straight leg raise. Lift leg, heel toward sky. Stretch. return to start. Alternate legs, 5-10 each.

AlliUltra

The Healing Power of Garlic in a Super-Potent Liquid Extract.

AlliUltra® Liquidium

Each bottle contains:
15ml Allisure® AC-23 stabilized allicin liquid in a water base.

AlliUltra™ Allisure® AC-23 Liquidium is made from fresh, raw garlic. Heads of garlic are specifically selected to ensure that they contain significant enzyme activity (allinase enzyme). Garlic heads are split into cloves, which are left unpeeled and then subjected to crushing, filtration and a temperature controlled extraction process designed to produce pure liquid allicin dissolved in water. No chemical solvents are used. The allicin amino acid in fresh garlic is subjected to complete conversion by the allinase enzyme and to ensure a large volume of active allicin is harvested. The volume of allicin produced is directly related to the enzymatic activity.

Garlic is a natural antibiotic. Albert Schweitzer used garlic to treat dysentery in Africa. In addition to it’s broad-spectrum antimicrobial activity, garlic enhances numerous aspects of immune function. Garlic lowers blood pressure, triglycerides, and platelet stickiness (which can lead to clots and strokes while increasing HDL (the good cholesterol) and fibrinolysis (the breakdown of fibrin clots). Garlic is useful in HIV/AIDS, allergy, atherosclerosis, cancer, candidiasis, cardiac arrhythmias, diabetes type II, high blood pressure and infection.

Alliin, the primary substance of garlic, and alliinase, the activating enzyme, are present in separate chambers of the garlic clove. When garlic is ruptured, alliinase interacts with alliin and converts it to allicin – one of garlic’s most beneficial compounds. However, allicin dissipates quickly during standard processing techniques.

AlliUltra can also be used topically (externally) to help resolve any condition that has a bacterial, fungal or viral cause.

AlliUltra® Liquidium – Product # N316 (15 ml) $49.97
Each bottle contains 15ml Allisure® AC-23 stabilized allicin liquid in a water base.

Suggested Use: 1-8 drops per day—either internally or externally—for maximum health benefits.
Once opened AlliUltra should be kept refrigerated.

Enter Quantity Desired and Click “Add To Cart” Button

If you are pregnant, lactating, or using anticoagulants (including aspirin), please consult your healthcare professional prior to use. Also, do not use in children under 10 years of age unless recommended by a healthcare professional.

HYPOTHYROID (LOW THYROID FUNCTION)

Natural Support Strategies

Hypothyroid is a term that refers to low thyroid function. The condition can be either “primary” or “secondary.” Primary hypothyroidism means that the thyroid gland is not producing enough thyroid hormone. “Secondary” (also called sub-clinical) hypothyroidism means that the thyroid gland is producing a normal amount of thyroid hormone but it is not being converted to its more active form in the liver or the “target” tissues. Primary hypothyroidism is diagnosed by a blood test. (TSH is the screening blood test for thyroid function). Secondary hypothyroidism is determined by symptoms and basal body temperature.

Symptoms of low thyroid function include cold intolerance, fatigue, anemia, difficulty losing weight, menstrual disorders, memory and concentration difficulties, constipation, infertility, dry skin, elevated cholesterol levels, depression, muscle and joint stiffness to name just a few. Because thyroid hormone sets the “pace” for all cells in the body, a deficiency can result in “sluggishness” of virtually any physical function.

Because the body temperatures will be low in both primary and secondary low thyroid, basal body temperatures are a sensitive self-test to evaluate thyroid function. If you have thyroid symptoms or your temperature is low, get a thyroid blood test to see if the gland is producing sufficient thyroid hormone. These tests usually require a doctor’s order. Primary low thyroid usually requires prescription thyroid medication (preferably natural thyroid hormone) for correction. Secondary low thyroid can be corrected by self-help measures.

Thyroid hormones are made in the body from iodine. the T4 thyroid hormone contains 4 iodine molecules, and T3 contains 3 iodine molecules. Anyone with primary or secondary low thyroid should have an iodine test to determine iodine levels.

DIET AND LIFESTYLE RECOMMENDATIONS

  • Exercise regularly. Lack of physical activity is a common cause of secondary low thyroid function.
  • Iodine test. Both low iodine and excess iodine impede thyroid function. Be careful of taking excess iodine in supplemental form until the results of an iodine test are available.
  • Diet. Use sea salt or natural unrefined salt which contains iodine and other minerals necessary to normal thyroid function
  • Avoid bromine. Bromine is a mineral which displaces iodine from the thyroid gland, impairing thyroid function. it is used in baked goods as a dough conditioner, in some soda pops and other foods. Read labels.

PRIMARY SUPPORT

  • Maxi Multi: 3 caps, 3 times per day with meals. Optimal (not minimal) doses of vitamins A, C, E, B2, B3, B6, zinc, and selenium are particularly important for correcting hypothyroidism.
  • Iodoral (Iodine) amount based on iodine test results, typically 1-4 tabs or as directed by healthcare professional.
    OR
  • Modifilan (seaweed source of natural iodine) 4-6 caps per day. Provides a highly bio-available source of iodine plus detoxifying co-factors. Can be safely taken by most people even without an iodine test.

ADDITIONAL SUPPORT

  • Milk Thistle Plus: 1-2 caps, 3 times per day with meals. This improves the liver’s ability to convert thyroid hormone (T4) to its more active form (T3).
  • Thyroid cytotrophin: 1-2 tabs daily or as directed by healthcare professional.

Learn more about the importance of iodine in Iodine: the “Missing Mineral” for Thyroid, Heart, Healthy Immunity and Cancer Protection