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Meschino Health Comprehensive Guide to Herbs
Table of Contents
INTRODUCTION ........................................................................................................................................................................ 1 TABLE OF CONTENTS ................................................................................................................................................................ 2 ABOUT MESCHINO HEALTH COMPREHENSIVE GUIDE TO VITAMINS ......................................................................................... 4 MESCHINO HEALTH NATURAL HEALTH ASSESSMENT ............................................................................................................... 5 ALOE VERA ............................................................................................................................................................................... 6 ANGELICA SPECIES .................................................................................................................................................................... 9 ASTRAGALUS .......................................................................................................................................................................... 11 BACOPA .................................................................................................................................................................................. 15 BETA SITOSTEROL ................................................................................................................................................................... 17 BILBERRY ................................................................................................................................................................................ 20 BLACK COHOSH ...................................................................................................................................................................... 24 BOSWELLIA ............................................................................................................................................................................. 28 BROMELAIN ............................................................................................................................................................................ 31 CAPSICUM .............................................................................................................................................................................. 36 CERNITIN POLLEN EXTRACT .................................................................................................................................................... 39 CHASTE TREE .......................................................................................................................................................................... 42 CHINESE SKULL CAP ................................................................................................................................................................ 45 COLEUS FORSKOHLII (FORSKOLIN) .......................................................................................................................................... 50 CRANBERRY ......................................................................................................................................................................... 544 DANDELION (TARAXACUM OFFICINALE) ................................................................................................................................. 57 DEVILS CLAW ......................................................................................................................................................................... 59 ECHINACEA (PURPLE CONEFLOWER)....................................................................................................................................... 62 EPHEDRA ................................................................................................................................................................................ 66 FEVERFEW .............................................................................................................................................................................. 70 FLAXSEED AND FLAXSEED POWDER ....................................................................................................................................... 73 GARLIC (ALLIUM SATIVUM) .................................................................................................................................................... 78 GINGER ................................................................................................................................................................................... 83 GINKGO BILOBA...................................................................................................................................................................... 87 GINSENG ................................................................................................................................................................................. 93 GOLDENSEAL (HYDRASTIS CANADENSIS) ................................................................................................................................ 99 GOTU KOLA (CENTELLA ASIATICA) ........................................................................................................................................ 102
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Meschino Health Comprehensive Guide to Herbs
GUGULIPID (GUM GUGGUL) ................................................................................................................................................ 106 HAWTHORN (CRATAEGUS OXYACANTHA) ............................................................................................................................ 110 HORSECHESTNUT SEED (AESCULUS HIPPOCASTANUM) ........................................................................................................ 115 HUPERZINE A ........................................................................................................................................................................ 119 KAVA (PIPER METHYSTICUM) ............................................................................................................................................... 122 LICORICE (GLYCYRRHIZA GLABRA) ........................................................................................................................................ 127 MILK THISTLE (SILYBUM MARIANUM) ................................................................................................................................ 1333 MUIRA PUAMA (POTENCY WOOD) ................................................................................................................................... 13939 PICRORHIZA ...................................................................................................................................................................... 14141 PYGEUM (PYGEUM AFRICANUM) ..................................................................................................................................... 14545 RED CLOVER (TRIFOLIUM PRATENSE) ............................................................................................................................... 14848 REISHI MUSHROOM EXTRACT........................................................................................................................................... 15353 SAW PALMETTO (SERENOA REPENS) ................................................................................................................................ 15858 SHIITAKE MUSHROOM ....................................................................................................................................................... 1644 ST. JOHNS WORT (HYPERICUM PERFORATUM) ................................................................................................................ 16767 STINGING NETTLE OR NETTLE (URTICA DIOICA) ................................................................................................................ 17373 TRIBULUS TERRESTRIS (PUNCTURE VINE) ......................................................................................................................... 17777 TURMERIC (CURCUMIN) ................................................................................................................................................... 17979 UVA URSI (BEARBERRY) .................................................................................................................................................... 18383 VALERIAN (VALERIANA OFFICINALIS) ................................................................................................................................ 18585 VINPOCETINE .................................................................................................................................................................... 18989 WHITE WILLOW BARK (SALIX SPP) .................................................................................................................................... 19292 WILD YAM (DIOSCOREA VILLOSA) ......................................................................................................................................... 196
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Meschino Health Comprehensive Guide to Herbs
All four books were written to both educate and provide an easy to use quick reference to answer important questions regarding nutrients. Users of the guide can quickly find which health conditions the nutrient can impact, proper dosage, possible effects of a deficiency or the effect any potential toxicity associated with the nutrient. Finally any drug-nutrient Interactions associated with the nutrient. More eBook and eQuick Guides Meschino Health is excited to be able to provide tools and resources to help you achieve your healthy living objectives. Sharing the Healthy Living message and helping anyone who is interested in living a healthy happy life is what Meschino Health is all about. Visit www.MeschinoHealth.com to learn the latest a science based research on diet and supplementation that can prevent and treat health conditions often associated with aging. New eBooks and eGuides are added every month and can be downloaded free of charge.
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Meschino Health Comprehensive Guide to Herbs
Easy to Complete Online Questionnaire Your Personal Health Assessment is generated Instantly and can be downloaded to your computer The Meschino Health Assessment is a 15 to 20 page comprehensive report complete with diet, lifestyle and supplement considerations that are specific to your profile.
The Meschino Health Assessment is a free service created by Dr. James Meschino. The feedback in your report is based on your answers to the questions in the Health Assessment, and highlights the dietary, lifestyle and supplementation practices that are best suited to your circumstances, according to currently available scientific studies The Meschino Health Assessment is a Free Service
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Meschino Health Comprehensive Guide to Herbs
Aloe Vera
General Features
Aloe Vera is a perennial plant with yellow flowers. The leaves contain active ingredients, including the polysaccharide acemannan and anthraquinones.1 Aloe Vera gel and juice has been used therapeutically for the treatment of peptic ulcers and other intestinal disturbances, including its use as a natural laxative. Aloe Vera gel can also be applied topically to aid in the healing of burns, wounds, and other skin conditions.4
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Meschino Health Comprehensive Guide to Herbs
Topical Dosage
Aloe Vera Gel can be applied liberally for topical applications.3 The usual application for the skin lesions noted above is three times per day, using a 0.5% Aloe Vera cream.8,9,10
Drug-Nutrient Interactions
Laxative Effect as Aloe Vera is known to act as a laxative it may reduce the absorption of medications, if taken at the same time. Thus, other medications and supplements should not be taken at the same time as Aloe Vera ingestion. 7
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1. 2. 3. 4. 5. 6. 7. 8.
Sheltom RW, Aloe Vera, Its Chemical and Therapeutic Properties, Int J Dermatol 1991;30:679-83. Blitz JJ, Smith JW, and Gerard JR, Aloe Vera Gel in Peptic Ulcer Therapy: Preliminary Report, J Am Osteopathol Soc 1963;62:731-5. Davis RH, Kabbani JM, and Maro NP, Aloe and Wound Healing, J Am Pod Med Assoc 1987;77:165-9. Dietary Supplement Information Bureau. www.content.intramedicine.com: Aloe Vera. Collins CE, et al. Roentgen dermatitis treated with fresh whole leaf Aloe vera. Am J Roentgenol.1935; 33: 396-97. Chithra P et al. Influence of Aloe Vera on collagen characteristics in healing wounds in rats. Mol Cell Biochem. 1998; 181 (I-2): 71-6. Ishii Y, et al. Studies of Aloe .III. Mechanism of cathartic effect. (2). Chem Pharm Bull.Tokyo.1990; 38 (1): 197-200. Syed TA, Cheeman KM, Ashfaq A, et al. Aloe Vera extract 0.5% in a hydrophilic cream versus Aloe Vera gel for the management of genital herpes in males. A placebo-controlled, double-blind, comparative study. J Eur Acad Detmatol Venereol. 1996;7: 294-95. 9. 9 Syed TA, Ahmed SA, Holt AH, et al. Management of psoriasis with Aloe Vera extract in a hydrophilic cream: a placebo-controlled, double blind study. Trop Med Int Health. 1996; 1: 505-509. 10. 10 Vardy DA, Cohen AD, Tchetov T, et al. A double-blind, placebo-controlled trial of Aloe Vera emulsion in the treatment of seborrheic dermatitis. J Dermatol Treat. 1999; 10: 7-11.
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Meschino Health Comprehensive Guide to Herbs
Drug-Nutrient Interactions
Anticoagulants (warfarin, coumadin, aspirin etc) animal studies demonstrate that Angelica Species potentiates the anti-clotting effects of warfarin and thereby, may increase the chance of a serious bleeding disorder. Several reports of this consequence in humans have been reported, even in women not taking concurrent anticoagulant therapy. Therefore, women should not take Dong Quai concurrently with any anticoagulant drug.6,7,8,9 (note that Black Cohosh, Soy Isoflavones, Gamma Oryzanol and Chasteberry are not associated with this risk).
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Meschino Health Comprehensive Guide to Herbs
Astragalus
General Features
Astragalus has been used for at least 2000 years in China and continues to be widely used as a herb that is known to enhance function of the immune system and facilitates an increase in energy production within the heart muscle, in cases where certain forms of heart disease exist.1,2,3,4,5 It is one of the most widely used herbs in Fu-zheng therapy the use of herbs to augment the host defense mechanisms. 1,2,3,6 Astragalus is a herbaceous perennial with the root of the plant used for medicinal purposes.7
Active Constituents
These primarily include: 1. Triterpene glycosides (saponins): astragalosides, etc. 2. Polysaccharides: astragalans 3. Flavonoids7,8,9,10,11
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congestive heart failure demonstrate improvement in chest distress, dyspnea (shortness of breath), exercise tolerance and other parameters of cardiac function, when given Astragalus intravenously. 10,24 Astragalus has also been used effectively in patients suffering from ischemic heart disease 25 and it has been shown to increase cardiac output in 20 patients with angina pectoris.26 3. Anti-Cancer Effects The immune- enhancing effects of Astragalus make this herb an interesting compound in terms of its potential in cancer treatment. A clinical study of 54 patients with small cell lung cancer were treated with regular medical interventions plus Traditional Chinese Medicine (including Astragalus). Increased survival was noted in comparison to the average survival statistics of conventional medicine alone.27 Animal studies demonstrate quite strongly that Astragalus has the potential to prevent some cancers and has curative potential in others (e.g., renal cell carcinome model in mice).28,29 Intensive research continues in an attempt to establish the true anti-tumor potential of Astragalus. 4. Male Fertility Astragalus has been shown to significantly increase the motility of human sperm in vitro. 30 This may be of value in the treatment of male infertility where poor sperm motility is a suspected factor. Note that L-carnitine and zinc supplementation have demonstrated similar capabilities (see details in this document under their individual headings.)
Drug-Nutrient Interactions
Immunosuppressive Medications As Astragalus has been shown to enhance immune function, it may counter the efficacy of immnosuppressive drugs.32,33
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Foster S, ChongxlY. Herbal Emissaries. Bringing Chinese Herbs to the West. Rochester, VT; Healing Arts Press, 1992:p356 Zhao KS, Manoinin C, Doria G. Enhancement of the immune response in mice by Astragalus membranaceous extracts. Immunopharmacology. 1990:20(3):225-233 Sun, Y, et al. Preliminary observations on the effects of the Chinese medicinal herbs Astragalus membranaceous and Ligustrum lucid on lymphocyte blastogenic responses. Journal of Biological Response Modifiers. 1983;2:227-237 Geng CS, et al. Advances in Immuno-pharmacological Studies on Astragalus membranaceous. Chung, Hsi i Chieh Ho Tsa Chih. 1986;6(1):62-64 Chen, LX, Liao, JX., Guo, WQ. Effects of Astragalus membranaceous on left Ventribular Function and Oxygen Free Radical in Acute Myocardial Infarction Patients and Mechanism of its Cardiotonic Action. Chung Kuo, Chung Hsi, I Chieh Ho Tsa Chih. Mar 1995;15 (3):1413 Sun Y, Change YH, Uy Gq, et al. Effect of Fu-zheng therapy in the management of malignant diseases. Chinese Med Journal, 1981;61:97101 Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs, and Cosmetics. 2nd ed. Toronto/New York: John Wiley and Sons Inc;1996:p649 Chevallier A. The Encyclopedia of Medicnal Plants. London: Readers Digest;1996:p336 Zhao, K W, Kong, HY. Effect of Astragalan on secretion of tumour necrosis factor in human peripheral blood monomuclear cells. Chung-Kuo Chung Hsi i Chieh, Ho Tsa Chih. 1993 Luo HM, Dai RH, Li Y. Nuclear cardiology study on effective ingredients of Astragalus membranaceous in treating heart failure. Chung-Kuo Chung His i Chieh, Ho Tsa Chih. 1995; 15(12):709-9 Hirotani M, Zhou Y, Rui H, Furuya T. Cycloartane triterpene glycosides from the hairy root cultures of Astragalus membranaceous. Phytochemistry. 1994;37(5):1403-7 Weng XS. Treatment of leucopenia with pure Astragalus preparation an analysis of 115 leucopenic cases 9Chinese). Chung-Kuo Chung Hsi i Chieh, Ho Tsa Chih. 1995;15(8):462-4 Chu, DT et al. Immunotherapy with Chinese medicinal herbs. II. Reversal of cyclophosphamide-induced immune suppression by administration of fractionated Astragalus membranaceus in vivo. Journal of Clinical Laboratory Immunology. 1988;25:125-129 Chen YC. Experimental studies on the effects of danggui buxue decoction on IL-2 production of blood-deficient mice (Chinese). Chung-Kuo Chung Hsi i Chieh. 1994; 19(12): p739-41,p763 Liang H, Zhang Y, Geng B. The effect of Astragalus polysaccharides (APS) on cell medicated immunity (GMI) in burned mice. Chung-Hua Cheng Hsing Shao Shang Wai Ko Tsa Chih.
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16. Hou YD, Ma GL, Wu SH, Li HT. Effect of radix Astrageli seu Hedysari on the interferon system. Chinese Medical Journal. 1981;94:35-40 17. Jin R, Wan LL, Mitsuishi T. Effects of shi-ka-ron and Chinese herbs in mice treated with anti-tumor agent mito mycin C (Chinese). ChungKuo Chung Hsi i Chieh, Ho Tsa Chih. 1995;15(2):101-3 18. Sugiura H, Nishida H, Indaba R, Iwata H. Effects of exercise in the growing stage in mice and of Astragalus membranaceous on immune functions (Japanese). Nippon Eiseigaku Zasshi Japanese Journal of hygiene, 1993;47(6):1021-31 19. Yang YZ, Jin PY, Guo Q, et al. Effect of Astragalus membranaceous on natural killer cell activity and induction of a- and g- interferon in patients with coxsackie B viral myocarditis. Chinese Medical Journal 1990;103(4):304-307 20. Yang YZ, Guo Q, Jin PY, et al. Effect of Astragalus membranaceous injection on Coxsackie B-2 virus infected rat beating heart cell culture. Chinese Medical Journal. 1987;100-595 21. Hou YD. Study on the biological active ingredients of Astragalus membranaceous. Chung His i Chieh Ho Tsa Chih. 1984;4:p420 22. Zhang Xq, et al. Studies of Astragalus membranaceous on antiinfluenza virus activity, interferon induction and immunostimulation in mice. Chinese Journal of Microbiology and Immunology. 1984;4:p92 23. Research Group of Common Cold and Bronchitis. Investigation into Astragalus membranaceous. II. A research on some of its mechanism of reinforcing the Qi (vital energy.) Journal of Traditional Chinese Medicine. 1980;3:p67 24. Shi HM, Dai RH, Fan WH. Intervention of lidocaine and Astragalus membranaceous on ventricular late potentials (Chinese). Chung-Kuo Chung Hsi i Chieh, Ho Tsa Chih. 1994;14 (10):598-600 25. Li SQ, Yuan RX, Gao H. Clinical observation of the treatment of ischemic heart disease with Astragalus membranaceous (Chinese). ChungKuo Chung Hsi i Chieh, Ho Tsa Chih. 1995;15(2):77-80 26. Lei ZY, Qin H, Liao JZ. Action of Astragalus membranaceous on left ventricular function of antina pectoris (Chinese). Chung-Kuo Chung Hsi I Chieh, Ho Tsa Chih. 1994;14(4):199-202 27. Cha RJ, Zeng DW, Chang QS. Non-surgical treatment of small cell lung cancer with chemo-radio-immunotherapy and traditional Chinese medicine (Chinese). Chung-Hua Nei Ko Tsa Chih Chinese Journal of Internal medicine. 1994;33(7):462-6 28. Lau BH, Ruckle HC, Botolazzo T, Lui, PD. Chinese medicinal herbs inhibit growth of murine renal cell carcinoma. Cancer Biotherapy. 1994;9(2):153-61 29. Chu DT, Lin JR, Wong W. The in vitro potentiation of LAK cell cytotoxidicty in cancer and AIDS patients induced by F3 a fractionated extract of Astragalus membranaceous (Chinese). Chung-Hun Chung Liu Tsa Chih Chinese Journal of Oncology. 1994;16(3):167-71 30. Hong C, Ku J, et al. Astragalus membranaceous stimulates human sperm motility in vitro. American journal of Chinese Medicine. 1992;20:289-94 31. Murray MT. The Healing Power of Herbs. Rocklin, CA: Prima Publishing;1992:p246 32. Zhao KS, et al. Enhancement of the Immune Response in Mice by Astragalus membranaceous Extracts. Immunopharmacology. 1990;20(3):225-33 33. Chu, DT, et al. Immune Resoration of Local Xenogeneic Graft-versus-host Reaction in Cancer Patients in In-vitro and Reversal of Cyclophosphamide-induced Immune suppression in the Rat in Vivo by Fractionated Astragalus membranaceous. Chung Hsi i Chieh Ho Tsa Chih. Jun 1989;9:351-54.
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Active Constituents
The primary active constituents include Bacosides A and B.1 The alcohol fraction of Bacopa extract has been shown to provide its strong antioxidant properties.2
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Meschino Health Comprehensive Guide to Herbs
During pregnancy and lactation, the only supplements that are considered safe include standard prenatal vitamin and mineral supplements. All other supplements or dose alterations may pose a threat to the developing fetus and there is generally insufficient evidence at this time to determine an absolute level of safety for most dietary supplements other than a prenatal supplement. Any supplementation practices beyond a prenatal supplement should involve the cooperation of the attending physician (e.g., magnesium and the treatment of preeclampsia.)
1. 2. 3. 4. 1. 2. 3.
1. Encyclopedia of Nutritional Supplements. Murray M. Prima Publishing 1998. 2. Reavley NM. The New Encyclopedia of Vitamins, Minerals, Supplements, and Herbs. Evans and Company Inc. 1998. 3. The Healing Power of Herbs (2nd edition). Murray M. Prima Publishing 1995. 4. Boon H and Smith M. Health Care Professional Training Program in Complementary Medicine. Institute of Applied Complementary Medicine Inc. 1997.
Encyclopedia of Nutritional Supplements. Murray M. Prima Publishing 1998. Reavley NM. The New Encyclopedia of Vitamins, Minerals, Supplements, and Herbs. Evans and Company Inc. 1998. The Healing Power of Herbs (2nd edition). Murray M. Prima Publishing 1995. Boon H and Smith M. Health Care Professional Training Program in Complementary Medicine. Institute of Applied Complementary Medicine Inc. 1997.
Dietary Supplement Information Bureau. www.content.intramedicine.com: Bacopa monnieri Tripathi YB et al. Bacopa monniera linn. As an antioxidant: Mechanism of action. Indian J Exp Biol. Jun1996;34(6):523-6 Kidd PM. A review of nutrients and botanicals in the integrative management of cognitive dysfunction. Altern Med Rev. Jun1999;4(3):144-61 4. Stough C, Lloyd J, Clarke J, Downey LA, Hutchison CW, Rodgers T, et la. The chronic effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy human subjects. Psychopharmacology (Berl), Aug2001;156(4):481-4 5. Mukherjee GD et al. Clinical trial on brahmi. I. J Exp Med Sci, 1966;10(1):5-11 6. Vohora D, Pal SN, Pillai KK. Protection from phenbytoin-induced cognitive deficit by Bacopa monniera, a reputed Indian nootropic plant. J Ethnopharmacol, Aug2000;71(3):383-90 7. Dar A, Channa S. Calcium antagonistic activity of Bacopa monniera on vascular intestinal smooth muscles of rabbit and ginea-pig. J Ethnopharmacol, 1999;66(2):167-74
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Meschino Health Comprehensive Guide to Herbs
Beta Sitosterol
General Features
Phytosterols or plant sterols are structurally similar to cholesterol. The most common plant sterols are beta-sitosterol, campesterol and stigmasterol. Epidemiological and experimental studies suggest that dietary phytosterols may offer protection from the most common cancers in Western societies, such as colon, breast and prostate cancer. Phytosterols have been shown to behave as protective nutrients via a number of physiological effects, including their effect on cell membrane structure and function of tumor and host tissue, signal transduction pathways that regulate tumor growth and apoptosis (programmed cell death), immune function and cholesterol metabolism.
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3. Autoimmune Diseases (including Rheumatoid Arthritis) Evidence points to the fact that certain phytosterols selectively stimulate activity of Th1-helper cells and suppress activity of Th2-helper cells. This modulation of the immune system is related to a reduction in inflammatory processes and improved immune system function.9 4. Immune System Support (including HIV-Infection) A clinical trial involving eighty patients with HIV-infection was conducted over 36 months. Supplementation with sterols/sterolins demonstrated that it may slow the progression of the disease due to its modulating effects on the immune system.10 Some evidence also exists to show that supplementation with beta-sitosterol and beta-sitosterol glucoside enhances immune system parameters in patients with pulmonary tuberculosis. Supplemented patients experienced improved weight gain, and higher lymphocyte and eosinophil counts compared to the placebo group. 11
Dosage Ranges
1. Benign Prostatic Hyperplasia - 20 mg beta-sitosterol, three times per day or 65 mg beta-sitosterol, twice per day.4,5,7,8 2. Cholesterol Lowering - 500 mg to 10,000 mg per day of beta-sitosterol.2,3 3. Autoimmune Diseases - 1 capsule sterinol, three times daily on an empty stomach.12 (i.e., Moducare) 4. HIV and Tuberculosis Infection - 2 capsules of sterinol, three times a day for one week, and 1 capsule, three times a day for maintenance13 (i.e., Moducare). Other infectious diseases may also be aided with sterinol supplementation.13
Drug-Nutrient Interactions
There are no well-known drug-nutrient interactions with beta-sitosterol.14
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Ostland RE,(Jr), et al. Sitostanol administration in lecithin micelles potently reduces cholesterol absorption in humans. Am J Clin Nutr. 1999; 70: 826-831.
Awad, AB, et.al., Phytosterols as Anticancer Dietary Components: Evidence and Mechanism of Action, J Nutr 2000;130:2127-30. Lees, AM, et.al., Plant Sterols as Cholesterol-lowering Agents: Clinical Trials in Patients with Hypercholesterolemia and Studies of Sterol Balance, Atheroscles 1997;28:325-38. Pelletier, X, et.al., A Diet Moderately Enriched in Phytosterols Lowers Plasma Cholesterol Concentrations in Normocholesterolemic Humans, Ann Nurt. Metab 1995;39:291-5. Berger, RR, et.al., Randomised, Placebo-controlled, Double-blind Clinical Trial of Beta-sitosterol in Patients with Benign Prostatic Hyperplasia, Lancet 1995;345:1429-532. Klippel, KF, et.al., A Multicentric, Placebo-controlled Double-blind Clinical Trial of Beta-sitosterol for the Treatment of Benign Prostatic Hyperplasia, Br J Urol, 1997;80:427-432. Bouic, PJ, et.al., Plant Sterols and Sterolins: A Review of Their Immune-modulating Properties, Altern Med Rev 1999;3:170-7. Berger, R, et.al., Treatment of Symptomatic Benign Prostatic Hyperplasia with Beta-sitosterol, an 18-month Follow-up, Br J Urol 2000;85(7):842-6. Wilt, TJ, et.al., Beta-sitosterol for the Treatment of Benign Prostatic Hyperplasia: A Systematic Review, BR J Urol Int. 1999;83(9):976-83. Pegel, KH, The Importance of Sitosterol and Sitosterolin in Human and Animal Nutrition, South African J Sci. 1997;93:263-8. Bouic, P, Immunomodulation in HIV/AIDS: The Typerberg:/Stellenbosch University Experience, Bouic, P AIDS Bulletin, 1997;6:18-20. Donald, PR, et.al., A Randomized, Placebo-controlled Trial of the Efficacy of Beta-sitosterol and its Glucoside as Adjuvants in the Treatment of Pulmonary Tuberculosis, Int J Tuberc Lung Dis. 1999;1(5):518-22. Vanderhaeghe, L and Bouic P, The Immune System Cure, Prentice-Hall Canada Inc, 1999:125-55. Vanderhaeghe, L and Bouic P, The Immune System Cure, Prentice-Hall Canada Inc, 1999:175-96. Healthnotes Online, Healthnotes 2000, Inc.
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Active Ingredients
Research has focused primarily upon the anthocyanosides, which are flavonoid compounds, unique to Bilberry extract. They are formed by an anthocyanidin backbone bound to one of three sugars (arabinose, glucose or galactose). The concentration of anthocyanosides in the fresh fruit is only 0.1 to 0.25 percent, whereas concentrated extracts of Bilberry taken as supplements yield an anthocyanidin content of 25 percent.1,2,3,21,22
Mechanism of Action
1. Collagen Stabilizing action Bilberry preserves collagen and related ground substance by increasing the cross-linking of collagen fibers, acting as a free radical scavenger, inhibiting enzymatic cleavage of collagen by enzymes secreted by leukocytes during inflammation, reducing the release of histamine, serine proteases, prostaglandins and leukotrienes and by promoting the synthesis of glycosaminoglycans (see glucosamine in this document) and collagen by chondrocytes.4,5,6,7 2. Anti-aggregation of platelets Like many other flavonoids anthocyanosides heve been shown to decrease platelet aggregation in experimental studies.8,9,10 3. Antioxidant The anthocyanodins derived from Bilberry also demonstrate very potent antioxidant properties.4
Clinical Applications
1. Macular Degeneration of the Eye Macular degeneration is the most common cause of blindness in individuals over the age of 55 (see also Lutein and Zeazanthin in this document) in North America. Bilberry anthocyanidins appear to be able to help defend against and manage macular degeneration and other eye conditions via several biological actions. The first is that these unique flavonoids have been shown to improve the delivery of oxygen and blood to the eye. The second is that they provide antioxidant protection against ultra-violet light induced free radical damage (from sunlight) to the macula of the eye, which has been shown to contribute to the development and progression of macular degeneration. Third, anthocyanidins from Bilberry have been shown to stabilize the blood vessel wall of small blood vessels in the macular region of the eye, helping to prevent leaking of blood (micro-hemorrhaging) into the macular region as often occurs in diabetic retinopathy and the wet form of macular degeneration. Like the antioxidant carotenoids lutein and zeazanthin, Bilberry anthocyanosides are known to concentrate in the macula of the eye, where they have the opportunity to quench ultra-violet light induced free radicals.21,22
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In one study, 31 patients with various retinopathies (20 diabetic, 5 retinitis pigmentosa, 4 macular degeneration, hemorrhagic retinopathy) were treated with Bilberry extract. There was a tendency toward reduced permeability and hemorrhage observed in all patients, especially in those with diabetic retinopathy.18 2. Cataract In the study by Bravetti G. (1989), Bilberry extract, plus vitamin E stopped progression of cataract formation in 97 percent of 50 patients with senile cortical cataracts. This effect is thought to be due to its powerful antioxidant properties, protecting the lens of the eye from oxidation and regenerating its collagen fibers. 17 3. Night Vision Bilberry anthocyanosides have an affinity for the pigmented epithelium or visual purple of the retina, which is the portion of the retina responsible for night vision (rhodopson pigment formed from vitamin A on the rods). The Royal Air Force pilots reported improved night vision during World War II with the use of Bilberry extract (also, quicker adjustment to darkness and faster recovery from glare). Even individuals with retinitis pigmentosa and hemeralopia (day blindness) have realized impressive improvement with Bilberry extract 11,12,13,14,15,16,17,18 supplementation. 4. Varicose Veins and Capillary Fragility Via its effects on collagen and connective tissues, which include increased synthesis of glycosaminoglycans (cement substance between fibers), reduced permeability and impaired prostaglandin synthesis, Bilberry has been used in clinical trials with capillary fragility problems. In one study, 47 patients with varicose veins treated with Bilberry extract (480 mg per day) witnessed significant improvement with edema, heaviness feeling, parethesia, pain and skin dystrophy.19,20 ( see also Horse chestnut and Grape seed extract in this document).
Drug-Nutrient Interactions
Anticoagulant Medications (e.g. warfarin, coumadin, aspirin) as Bilberry extract has been shown in experimental studies to reduce the clotting action of blood platelets, it may potentiate the action of other anticoagulant drugs. In these cases, prothrombin time (INR) should be monitored closely to guard against a possible bleeding disorder, although no human reports of such an occurrence have yet been reported.24
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Kuhnau J, The flavonoids, A Class of Semi-essential Food Components: Their Role in Human Nutrition, World Rev Nutr Diet 1976;24:117-91. Gabor M, Pharmacologic Effects of Flavonoids on Blood Vessels, Angiologica 1972;9:355-74. Havsteen B, Flavonoids, A Class of Natural Products of High Pharmacological Potency, Biochem Pharmacol 1983;32:1141-8. Monboisse JC, et. al. Non-enzymatic Degradation of Acid Soluble Calf Skin Collagen by Superoxide Ion: Protective Effect of Flavonoids, Biochem Pharmacol 1983;32:53-8. Monboisse JC, Braquet P, Borel JP. Oxygen-free Radicals as Mediators of Collagen Breakage. Agents Actions 1984;15:49-50. Rao CN, Rai VH, And Steinman B, Influence of Bioflavonoids on the Collagen Metabolism in Rats with Adjuvant Induced Arthritis. Ital J Biochem 1981;30:54-62. Ronziere MC, et. al., Influence of Some Flavonoids on Reticulation of Collagen Fibrils in Vitro. Biochem Pharmacol 1981;30:771-6. Middleton E, The Flavonoids, Trends Pharm Sci 1984;5:335-8. Amella M, et. al., Inhibition of Mass Cell Histamine Release by Flavonoids and Bioflavonoids. Planta Medica 1985;51:16-20. Jonadet M, et. al., Anthocyanosides Extracted from Vitis Vinifera, Vaccinium Myrtillus and Pinus Maritimus, I. Elastese-inhibiting Activities in Vitro, II. Compared Angioprotective Activities in Vivo, J Pharm Belg 1983;38:41-6. Detre A, et. al., Studies on Vascular Permeability in Hypertension: Action of Anthocyanosides. Clin Physiol Biochem 1986;4:143-9. Jayle GE and Aubert L, Action des Glucosides DAnthocyanes sur la Vision Scotopique et Mesopique du Sujet Normal Therapie 1964;19:171-85. Terrasse J and Moinade S, Premiers Resultats Obtenus Avec un Nouveau Facteur Vitaminique P les Anthocyanosides Extraits du Vaccinium Myrtillus, Presse Med 1964;72:397-400. Sala D, Rolando M, Rossi PL and Pissarello L, Effects of Anthocyanosides on Visual Performances at Low Illumination. Minerva Oftalmol 21, 283-285, 1979. Gloria E and Peria A, Effect of Anthocyanosides on the Absolute Visual Threshold, Ann Ottalmol Clin Ocul 1966;92:595-607. Junemann G, On the Effect of Anthocyanosides on Hemeralopia Following Quinine Poisoning. Klin Monatsbl Augenheilkd 1967;151:8916. Caselli L, Clinical and Electroretinographic Study on Activity of Anthocyanosides. Arch Med Int 1985;37:29-35. Wegman R, Maeda K, Troche P, and Bastide P. Effects of Anthocyanosides on Photoreceptors, Cytoenzymatic Aspects. Ann Histochim 1969;14:237-56. Bravetti G, Preventive Medical Treatment of Senile Cataract with Vitamin E and Anthocyanosides: Clinical Evaluation. Ann Ottalmol Clin Ocul 1989;115:109.
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18. Scharrer A and Ober M, Anthocyanosides in the Treatment of Retinopathies. Klin Monatbsl Augenheilkd 1981;178:386-9. 19. Mian E, et.al., Anthocyanosides and the Walls of Microvessels, Further Aspects of the Mechanism in the Action of their Protective Effect in Syndromes due to Abnormal Capillary Fragility. Minerva Med 1977;68:3565-81. 20. Ghiringhelli G, Gregoratti F, and Marastoni F, Capillarotropic Activity of the Anthocyanosides in High Doses in Phlebopathis Stasis. Min Cardioangiol 1978;26:255-76. 21. Murray MT, The Healing Power of Herbs (2nd edition), Prima Publishing, 1995. 22. Dietary Supplement Information Bureau. www.content.intramedicine.com: Bilberry 23. Jayle GE, et al. Study concerning the action of athocyanoside extracts of Vaccinium myrtillus on night vision. Ann Occul Paris. 1965; 198 (6): 556-62. 24. Moranzonni P, et al. Vaccinium myrtillus. Fitoterapia. 1996; vol LXVII (1): 3-29
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ratio described above. Thus, the use of Black Cohosh extract is proposed to provide relief of PMS in as much as its triterpene constituents can block the over-stimulation effect of the bodys more powerful estrogens and enable the body to increase its production of natural progesterone. Further, Black Cohosh triterpenes have also been shown to be anti-spasmodic, helping to reduce abdominal and uterine cramping associated with PMS. No other natural agent has been shown to provide all three of these biological actions, which appear to be of significance in the management of PMS.13,18 Other Female Conditions Preliminary trials suggest that Black Cohosh may provide benefit in other gynaecological complaints such as amenorrhea (both primary and secondary) dysmenorrhea, polymenorrhea, uterine fibroids, and fibrocystic breast disease.9,10,11
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Drug-Nutrient Interactions
There are no well-known drug interactions for black cohosh.15
Boon & Smith, Health Care Professional training program in complementary medicine, 39-43. Warnecke G. Beeinflussung klimakterisch beschwerden durch ein Phyto-terapeutikum, die medizinische welt 1985;36:871-4. Stolze H. An Alternative to treat menopausal complaints. Gyne 1982;3:1416. Wainecke G. Influencing menopausal symptoms with a phytotherapeutic agent. Med West 1985;36:871-4. Stoll W. Phytopharmacon influences atrophic vaginal epithelium, double-blind study, cimicifuga vs. estrogenic substances. Therapeuticum 1987;1:23-31. Daiber W. Menopause symptoms: success without hormones. Arztliche Praxis 1983;35:1946-7. Vorberg G. Treatment of menopause symptoms. ZFA 1984;60:626-9. Petho A. Menopause symptoms: is it possible to switch from hormone treatment to a botanical gynecologicum?. Arztliche Praxis 1987;47:1551-3. Schlidge E. Essay on the treatment of premenstrual and menopausal mood swings and depressive states. Rigelh Biol Umsch 1964;19(2):18-22. Brukes A. Essay on the phytotherapy of hormonal disorders in women. Med Welt 1960;44:2331-3. Gorlich W. Treatment of ovarian disorders in general practice. Arztl Praxis 1962;14:1742-3. Nesselhut T, et.al. Influence of cimicifuga vacemosa extracts with estrogen-like activity on the in vitro proliferation of mammary carcinoma cells. Institute of Tumor Immunology. Duderstadt, Germany, 1994. & Arch Gypecol Obstet 1993;254:817-8. Murray M and Pizzorno J, Encyclopedia of natural medicine. (revised 2nd edition). Prima Health 1998,639-41. Miksicek RJ. Commonly occurring plant flavonoids have estrogenic activity, moleculas. Pharmacology 1993;44:37-43. Blumenthal M, et.al. The complete commission E monographs. Austin, TX. American Botanical Council 1998:685. Bradley P. British herbal compendium. Gournemouth. BHMA 1992:239. Koin WD. Six-month oral toxicity study with remifemin: granulate in rats followed by an 8 week recovery peiod. Hannover, Germany. International Bioresearch 1991.
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18. Limon L. Use of alternative medicine in womens health. Am Pharmaceutical Assoc Annual Meeting. A Ph A, 2000. Pharmacists Conference Summaries 2000, Medscape Inc. 19. Healthnotes, Inc. 2001.www.healthnotes.com: Black Cohosh 20. Dietary Supplement Information Bureau. www.content.intramedicine.com: Black Cohosh
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Drug Interactions
There are no well-known drug interactions reported to date in regards to the use of Boswellia.5,6,7
1. 2. 3. 4. 5. 6.
Safayhi H, Sailer ER, Amnon HPT. 5-lipoxygenase inhibition by acetyl-11-keto-b-boswellic acid. Phytomed 1996;3:71-2. Safayhi H, Mack T, Saieraj J, et.al. Boswellic acids: novel, specific, nonredox inhibitors of 5-lipoxygenase. J Pharmacol Exp Ther 1992;261:1143-6. Etzel R. Special extract of Boswellia serrata (H15) in the treatment of rheumatoid arthritis. Phytomed 1996;3:91-4. Gupta I, Parihar A, Malhotra P, et.al. Effects of Boswellia serrata gum resin in patients with ulcerative colitis. Eur J Med Res 1997;2:37-43. Singh GB, Atal CK. Pharmacology of an extract of salai guggal ex-Boswellia serrata, a new non-steroidal anti-inflammatory agent. Agents Actions 1986;18: 407-12. Healthnotes Online, Healthnotes Inc., 1999.
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7. 8. 9.
10.
Dietary Supplement Information Bureau. www.content.intramedicine.com: Boswellia Gerhadt H, Seifert F, Buvari P, Vogelsang H, et al. Therapy of active Crohn disease with Boswellia serrata H 15. Gastroenterol. 2001; 39 (1): 11-7 Gupta I, Parihar A, Malhotra P, et al. Effects of gum resin of Boswellia serrata in patients with chronic colitis. Planta Med. 2001; 67 Safayhi H, et al. Inhibition by boswellic acids of human leukocyte elastase. J Pharmacol. Exp ther. 1997; 281 (1): 460-63
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Bromelain
General Features
Bromelain refers to a group of sulfur-containing enzymes that digest protein (proteolytic enzymes or proteases). Bromelain is derived from the stem of the pineapple plant (Ananas comosus).1 Experimental and clinical studies reveal that Bromelain exhibits anti-inflammatory properties, which include: a. Inhibition of the biosynthesis of pro-inflammatory prostaglandins and induction of prostaglandin E1 (which tends to inhibit inflammation) b. Activation of proteolytic activity at sites of inflammation and fibrinolysis activity via the plasminogen-plasmin system (Bromelain stimulates the conversion of plasminogen to plasmin, which in turn activates fibrinolytic activity, dissolving fibrin-based clots and reducing swelling). 2,3,4,5,6,7 c. Bromelain has also been shown to reduce plasma kininogen levels, which inhibits the production of kinins. Kinins are known to cause inflammation, swelling and pain.8 Human and animal studies verify that Bromelain, administered orally, is absorbed intact, from the gastrointestinal tract to the bloodstream (up to 40 percent absorption rate). 9,10,11 The human adult intestinal epithelium has traditionally been described as non-permeable to proteins. Recently, Castell, J.V., et al, demonstrated in the American Journal of Physiology (1997) that, after oral administration of Bromelain in 19 healthy men (oral multi-dosing of 3 gms per day), plasma concentrations reached as much as 5,000 pg/mL by 48 hours. From the plasma concentration curve, it could be estimated that an average of 10.8 micrograms of Bromelain was present in plasma in the 3-to-51 hour period. The presence of undegraded Bromelain in plasma was shown unequivocally by immunoprecipitation of plasma samples with antiBromelain antibodies, followed by gel electrophoresis and immunodetection. Moreover, the enzyme retained its biological activity.12
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In a recent double-blind clinical trial, 73 patients with gonarthritis were randomized to receive 3 weeks of treatment with an oral enzyme preparation, containing Bromelain, trypsin and rutin (n=36) or the NSAID diclofenac (n=37). Efficacy was primarily evaluated using the Lequesne index (measuring pain and function of the affected knee). Other investigations included assessment of pain symptoms using a visual analogue scale (VAS), global assessment of efficacy and tolerability (by both patients and one physician), and various laboratory parameters. Patients were evaluated at baseline, at weekly intervals throughout the 3-week treatment period, and at 7 weeks (i.e. 4 weeks after discontinuing therapy). The Lequesne index improved continuously in both groups: from 13.56 at baseline to 3.10 after 3 weeks (end of therapy) to 2.05 at 7 weeks (follow-up) in the enzyme group, and from 14.04 to 3.50 to 2.24 respectively, in the diclofenac group. The researchers conclude, short-term evaluation indicates that oral enzymes may be considered an effective and safe alternative to NSAIDs, such as diclofenac in the treatment of painful gonarthritis.14 Singer, et al, also reported anti-inflammatory activity of oral enzymes similar to that of diclofenac in patients with progressive gonarthritis.15 Klein, et al, demonstrated that proteolytic oral enzyme therapy was equally effective as was diclofenac in reducing pain in periarthritis of the shoulder in a clinical trial. Previously, these researchers had shown that proteolytic oral enzyme therapy was as effective as NSAIDs in reducing painful vertebral syndrome.16 2. Sports Injuries and Blunt Injuries to the Musculoskeletal System Dating back to the 1960s Bromelain has been used (oral administration) in the treatment of sports-related injuries. In one clinical trial, fifty-eight of seventy-four boxers receiving Bromelain reported that all signs of bruising had completely healed within 4 days. Of the remaining sixteen; complete healing took 8 to 10 days. Of the seventy-two controls, only ten showed complete resolution of healing by the fourth day, the remainder taking 7 to 14 days for complete healing to occur.17 The effect of orally administered Bromelain or the reduction of swelling, bruising, healing time, and pain following various surgical procedures has been demonstrated in several clinical studies. 6,18,19,20 In the study by Tassman, et al,18after oral surgery, swelling decreased within 3.8 days with Bromelain, compared with 7 days for the placebo in a double-blind study. In the same study, pain duration was reduced within 5.1 days in the Bromelain group, compared with 8.1 days in the placebo group. Recently, in an open case observation study involving patients with blunt injuries to the musculoskeletal system, the efficacy and tolerability of high-dose Bromelain was investigated by an orthopedic surgeon. In addition to usual therapeutic measures, 59 patients were treated with Bromelain preparations for one to three weeks based upon healing response. Treatment with Bromelain resulted in clear reduction of swelling, pain at rest and during movement, and tenderness to palpation. The addition of Bromelain to the treatment regime accelerated the rate of healing compared to the usual rate of healing observed for blunt injuries to the musculoskeletal system. The tolerability of the Bromelain preparation was very good, and patient compliance was correspondingly high.21 Experimental Investigations Demonstrating The Anti-inflammatory Properties of Bromelain Recent reviews have confirmed the analgesic, anti-inflammatory and edema-reducing properties of Bromelain and other proteolytic enzyme combinations.1,16 As reported by Kleef, et al, Bromelain-treated lymphocytes from healthy human donors displayed a 60 percent to 90 percent reduction in cell surface adhesion compared to untreated lymphocytes in vitro. The selective modulation of cell adhesion molecules may help explain some of the clinical effects observed after Bromelain treatment in patients suffering from chronic inflammatory disease, HIV and cancer.22
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Over the past few years, a number of studies have demonstrated the effects of oral enzymes, including Bromelain, on suppressing the synthesis of pro-inflammatory cytokines14,34 and adhesion molecules,22,35 the latter are expressed on the surface of cells, enabling cell-cell interactions, which are fundamental processes of the inflammatory reaction.36,37 In summary, oral enzyme therapy reduces various parameters of inflammation and pain by affecting the release of mediators of inflammation, modulation of adhesion molecules, reduction of immune complexes, activation of fibrinolysis and direct influences on nociceptors.14,16 3. Digestive Aid Bromelain in combination with other digestive enzymes and ox bile has been reported to help digest food 41, but is not generally used alone for this purpose.
Dosage
Anti-inflammatory: 250-750 mg, three times daily on an empty stomach. Bromelain is often standardize to 2,000 milk clotting units (MCU) which is 1333.3 Gelatin Dissolving Units (GDU) 38,47 Adverse Side Effects and Toxicity Currently, NSAIDs are first-line therapy in osteoarthritis. However, endoscopic studies have shown that lesions of the gastric mucosa developed in 14 to 31 percent of patients receiving long-term treatment with NSAIDs.23,24,25,26 In particular, the elderly may be seven times more likely to have silent ulcers from NSAID use.24,25,27,28 Other potential adverse effects of NSAIDs include cardiac, renal, hepatic and central nervous system damage.14 From an economic standpoint, the treatment of gastrointestinal adverse effects from NSAIDs has been calculated to add 45 percent to the cost of arthritis care. 29,30 By comparison, therapy with oral enzymes is not associated with severe gastrointestinal irritation, erosion, ulcerations, and related risks 14,1 and is generally well tolerated.14, 21,31,32,33 Determination of pepsinogen A and C, which are indicators of the function and morphological condition of the gastric mucosa, confirmed good gastric tolerability with administration of oral enzymes, including Bromelain.14 Unpublished data from trials of up to 4 years duration in patients with various clinical conditions (i.e. rheumatoid arthritis, multiple sclerosis) suggest that oral enzyme therapy, including Bromelain, is very well tolerated over longer periods.14 In regards to toxicity, animal studies have shown no toxic effects with Bromelain doses up to 10 grams per kilogram as no LD50 (50 percent lethal dose) exists for Bromelain doses in this range.38
Drug-Nutrient Interactions
1. Anticoagulant Medications (warfarin, coumadin etc) - In regards to potential adverse drug-nutrient interactions, studies using Bromelain on isolated human platelets in vitro revealed that Bromelain prevented thrombin-induced platelet aggregation, whereas papain enzyme was less active in preventing platelet aggregation. There is strong biological plausibility that Bromelain may further potentiate the anti-clotting influence of warfarin and coumadin, potentially increasing risk of a bleeding disorder. As well, animal studies and reports with humans indicate that Bromelain treatment can reduce thrombus formation via its thrombolytic action. To date there are no published reports of bleeding disorders occurring in humans using Bromelain supplementation. However, until more information is available, it is advisable to use caution and proper patient monitoring (prothrombin time, INR), when recommending Bromelain to patients on warfarin or anticoagulant therapy.39,40
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2. Antibiotics Bromelain has been shown to increase the amount of antibiotics in the blood and urine with concurrent orally administration.42,43,44,45,46
During pregnancy and lactation, the only supplements that are considered safe include standard prenatal vitamin and mineral supplements. All other supplements or dose alterations may pose a threat to the developing fetus and there is generally insufficient evidence at this time to determine an absolute level of safety for most dietary supplements other than a prenatal supplement. Any supplementation practices beyond a prenatal supplement should involve the cooperation of the attending physician (e.g., magnesium and the treatment of preeclampsia.) References: Pregnancy and Lactation 1. Encyclopedia of Nutritional Supplements. Murray M. Prima Publishing 1998. 2. Reavley NM. The New Encyclopedia of Vitamins, Minerals, Supplements, and Herbs. Evans and Company Inc. 1998. 3. The Healing Power of Herbs (2nd edition). Murray M. Prima Publishing 1995. 4. Boon H and Smith M. Health Care Professional Training Program in Complementary Medicine. Institute of Applied Complementary Medicine Inc. 1997. 1.
2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 5.. Tausssig SJ et al. Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharmacol. 1988;2:191-203 Ako H et al. Isolation of fibrinolysis enzyme activator from commercial Bromelain. Arch Int Pharmacodyn. 1981;254:157-67 Taussing S. The mechanism of the physiological action of Bromelain. Med Hypothesis 1980;6:99-104 Seligman B. Bromelain: an anti-inflammatory agent. Angiology. 1962;13:508-10 Pirotta F et al. Bromelain a deeper pharmacological study. Note I. Anti-inflammatory and serum fibrinolytic activity after oral administration in the rat. Drugs Exp Clin Res. 1978;4:1-20 Tassman G et al. Evaluation of a plant proteolytic enzyme for the control of inflammation and pain. J Dent Med 1964;19:3-77 Felton G. Does kinin released by pineapple stem Bromelain stimulate production of prostaglandin E1-like compounds? Hawaii Med J 1977;36:39-47 Katori M et al. A possible role of prostaglandins and bradykinin as a trigger of exudation in carrageenan-induced rat pleurisy. Agents Action 1978;8:108-12 Miller J et al. The increased proteolytic activity of human blood serum after oral administration of Bromelain. Exp Med Surg 1964;22:27780 Izaka K et al. Gastrointestinal absorption and anti-inflammatory effect of Bromelain. Jpn J Pharmacol 1972;22:519-34 Seifert J et al. Absorption of a proteolytic enzyme of plant origin from the gastro-intestinal tract into the blood and lymph of adult rats. Z Gastroenterol 1979;17:1-18 Castell JV et al. Intestinal absorption of undegraded proteins in men: presence of Bromelain in plasma after oral intake. Am J Physiol 1997;273:139-46 Cohen A et al. Bromelain therapy in rheumatoid arthritis. Pennsyl Med J 1964;67:27-30 Klein G et al. Short-term treatment of painful osteoarthritis of the knee with oral enzymes : A randomized, double-blind study versus diclofenac. Clin Drug Invest 2000;19 (1):15-23 Singer F et a. Therpie der aktivierten Arthrose: Zur effektivitat eines enzymgemisches versus diclofenac. Wien Med Wochenschr 1996;3:55-8 Klein G et al. Reducing pain by oral enzyme therapy in rheumatic diseases. Wein Med Wochenschr 1999;149:577-80 Blonstein J. Control of swelling in boxing injuries. Practitioner 1960:203-6 Tassman G et al. A Double-blind crossover study of a plant proteolytic enzyme in oral surgery. J Dent Med 1965;20:51-4 Howat R et al. The effect of Bromelain therapy on episiotomy wounds a double-blind controlled clinical trial. J Obstet Gynecol Br Common 1972;79:951-3 Ztuchni G et al. Bromelain therapy for the prevention of episiotomy pain. Obstet Gynecol 1967;29:275-8
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21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47.
Masson M. Bromelain in blunt injuries of the locomotor system. A study of observed application in general practice. Fortschr med 1995;113:303-6 Kleef R et al. Selective modulation of cell adhesion molecules of lymphocytes by Bromelain protease. Pathobiology 1996;64:339-46 Baskin WN et al. Aspirin-induced ultra structural changes in human gastric mucosa: correlation with potential difference. Ann Intern Med 1976;85:299-303 Miller DR. Treatment of nonsteroidal anti-inflammatory drug induced gastropathy. Clin Pharm 1992;11:690-704 Shallcross TM et al. Effect of nonsteroidal anti-inflammatory drugs on dyseptic symptoms. BMJ 1990;300:368-9 Soll AH et al. Nonsteroidal anti-inflammatory drugs and peptic ulcer disease. Ann Intern Med 1991;114:307-19 Clinch D et al. Absence of abdominal pain in elderly patients with peptic ulcers. Age Ageing 1984;13:120-3 Singh G et al. Gastrointestinal trct complications of nonsteroidal anti-inflammatory drug treatment in rheumatoid arthritis. A prospective observational cohort study. Arch Intern Med 1996;156:1530-6 Bloom BS. Direct medical costs of disease and gastrointestinal side effects during treatment for arthritis. Am J Med 1988;84 Suppl(2A):20-4 Green JM et al. Cost-conscious prescribing of nonsteroidal anti-inflammatory drugs for adults with arthritis. Arch Intern Med 1992;152:1995-2002 Miehlke K. Rheumabehandlung mit enzymen ist mehr als nur antiphlogistische therapie. In: Medizinische Enzym-Forschungsgesellschaft e.V.systemishe Enzym-therapie,15th working symposium, Munich, German. Grafelfing: Forum Medizin Verlag 1991 Miehlke K. Enyme minimieren Risiken der Rheymatherapie. In: Medizinische Enzym-Forschungs-gesellschaft e.V.Systemische Enzymtherapie, 10th working symposium, Franfurt, germany. Grafelfing: Forum Medizin Verlag, 1990 Gutfreund A et al. Effect of oral Bromelain on blood pressure and heart rate of hypertensive patients. Hawaii Med J 1978;37:143-6 Lehmann VP. Immunomodulation of proteolytic enzymes. Nephrol Dial Transplant 1996;9:253-63 Munzig E et al. Bromelain protease F9 reduces the CD44 mediated adhesion of human peripheral blood lymphocytes t human umbilical vein endothelial cells. FEBS Lett 1994;351:215-18 Mojcik C et al.Adhesion molecules. Arthritis Rheum 1997;40 :991-1004 Veale DJ et al. Cell adhesion molecules in rheumatoid arthritis. Drugs Aging. 1996;9:87-92 Murray M. The Healing Power of Herbs (2nd ed.) Prima Publishing 1995;Bromelain:60-9 Metzig C et al. Bromelain proteases reduce human platelet aggregation in vitro, adhesion bovine endothelial cells and thrombus formation in rat vessel in vivo. In Vivo 1999;13(1):7-12 Heck A. Potential interactions between alternative therapies an warfarin. Am J Health-Syst Pharm. 2000;57(13):1221-7 Balakrishnan V et al. Double-blind cross-over trial of an enzyme preparation in pancreatic steatorrhea. J. Assoc. Phys. Ind. 1981;29:2079 Tinozzie S, Venegoni A. Efect of Bromelain on serum and tissue levels of Amoxycillin. Drugs Exptl Clin Res. 1978;4:39-44 Renzinni G, Varengo M. The absorption of tetracycline in combination with Bromelain by oral application. Arzneim-Forsch. 1972;22:41012 Luerti M, Vignali ML. Influence of broemlain on penetration of antiobiotics in uterus, salpinx and ovary. Drugs Exp Clin Res. 1978;4:45-8 Bradbook ID et al. The effect of Bromelain on the absorption of orally administered tetracycline. Dr J Clin Pharmacol. Dec1978;6(6) :5524 Lucchi R et al. Chronic infections of the lower respiratory tract. Antibiotic therapy. Results of a double-blind study: tetracycline-HCL as monosubstance versus tetracycline and bromeline. ZFA (Stuttgart). Apr1980;56(11):807-12 Dietary Supplement Information Bureau. www.content.intramedicine.com:Bromelain
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Drug Interactions
There are no well- known drug-nutrient interactions for topical application of capsaicin creams.1 N.B.: Note that capsaicin is found in a variety of commercially available external analgesic preparations. 1
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1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.
Boon H, Smith M. Health care professional training program in complementary medicine. Institute of Applied Complementary Medicine Inc. 1997:53-60. Leung AY, Foster S. Encyclopedia of common natural ingredients used in food, drugs, and cosmetics. , 2 nd edition. Toronto/New York. John Wiley and Sons Inc. 1996:649. Tyler VE. Herbs of choice, the therapeutic use of Phytomedicinals. Binghamton, New York. Pharmaceutical Products Press 1994:2090. Locock RA. Capsicum. Canadian Pharmaceutical Journal 1985;118:517-9. Skofitsch G, Donnerer J, et.al. Comparison of nonivamide and capsaicin with regard to their pharmacokinetics and effects on sensory neurons. Arzneimittell Forsch 1984;341:154-6. Donofrio PD, Walker F, Hunt V, et.al. Treatment of painful diabetic neuropathy with topical capsaicin: a multicentre, double-blind, behicle-controlled study. Archives of Internal Medicine 1991;151:2225-9. Dailey GE. Effect of treatment with capsaicin on daily activities of patients with diabetic neuropathy. Diabetes Care 1992; 15(2):15965. Scheffler NM, et.al. Treatment of painful diabetic neuropathy with capsaicin 0.075%. Journal of the American Podiatric Medical Association 1991;81(6):288-93. Basha KM, Whitehouse FW. Capsaicin: a therapeutic option for painful diabetic neuropathy. Henry Ford Hospital Medical Journal 1991; 39(2):138-40. Pfeifer MA, et.al. A highly successful and novel model for treatment of chronic painful diabetic peripheral neuropathy. Diabetes Care 1993; 16(8):1103-15. Chad D, Ross D, Molitch M, et.al. Treatment of painful diabetic neuropathy with topical capsaicin a double-blind multicentre investigations. Pain 1990;42:387-8. Watson CP, et.al. Post-herpetic neuralgia and topical capsaicin. Pain 1988;35:289-97. Watson CP, Evans RJ, Wait VR, Birkett N. Post-herpetic neuralgia: 208 cases. Pain 1988;35:289-97. Bernstein JE, Korman NJ, Bickers DR, Dahl MV, Millikan LE. Topical capsaicin treatment of chronic postherpetic neuralgia. Journal of the American Academy of Dermatology 1989;21(2,Pt.1):265-70. Bernstein JE, Bickers DR, Dahl MV, Roshal JY. Treatment of chronic postherapetic neuralgia with topical capsaicin, a preliminary study. Journal of the American Academy of Dermatology 1987;17(1):93-6. Bernstein JE. Capsaicin in the treatment of dermatologic disease. Cutis 1987;39:352-3. Peikert A, Hentrich M, Ocas G. Topical 0.025% capsaicin in chronic post-herpetic neuralgia: efficacy, predictors of response and long-term course. Journal of Neurology 1991;238(8):452-6. Deal CL, Schnitzer TJ, Lipstein E, et.al. Treatment of arthritis with topical capsaicin: a double-blind trial. Clinical Therapeutics 1991;13(3):383-95. McCarthy G, McCarty D. Effect of topical capsaicin on asteoarthritis of the hands. Journal of Theumatology 1992;19:604-7. Sicuteri F, Fusco BM, Marabini S, et.al. Beneficial effect of capsaicin application to the nasal mucosa in cluster headache. Clinical Journal of Pain 1989;5:49-53. Marks DR, Rapoport A, Padla D, et.al. A double-blind, placebo-controlled trial of intranasal capsaicin for cluster headache. Cephalalgia 1993;13(20):114-6. Chesire WP, Snyder CR. Treatment of reflex sympathetic dystrophy with topical capsaicin. Pain 1990;43:307-11. Fuscu BM, Alessandri M. Analgesic effect of capsaicin in idiopathic trigeminal. Neuralgia, Anesthesia and Analgesia 1992;74(3):375-7. Watson CPN, Evans RJ, Watt VR. The post-mastectomy pain syndrome and the effect of topical capsaicin. Pain 1989;38:177-86. Watson CP, Evans RJ. The postmastectomy pain syndrome and topical capsaicin: a randomized trial. Pain 1992;51(3):375-9. Futrell JM, Tietschel RL. Spice allergy evaluated by results of patch tests. Cutis 1993;52:288-90. Niinimaki A, Hannuksela M, Makinen-Kiljunen S. Skin prick tests and in vitro immunoassays with native spices and spice extracts. Annals of Allergy, Asthma, & Immunology 1995;75:280-6.
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Dosage
BPH and Non Bacterial Prostatitis - a typical dosage is 63 mg, twice daily of cernitin pollen extract.1
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Drug-Nutrient Interactions
No drug-nutrient interactions for cernitin pollen extract are known at this time.2 NB: In Germany, phytotherapy is the primary treatment for mild to moderate urinary obstructive symptoms and represents more than 90 percent of all pharmaceuticals prescribed for the treatment of Benign Prostatic Hyperplasia. 2 A partial list of widely used Phytonutrients for Benign Prostatic Hyperplasia includes: Saw Palmetto Pygeum Africanum Beta-sitosterol Urtica dioica (stinging nettle) Cernitin pollen extract
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6.
Habib FK, et.al., In Vitro Evaluation of the Pollen Extract, Cernitin T-60, in the Regulation of Prostate Cell Growth, Br J Urol, 66, 1990, 393-397. 7. Ito R, et.al., Anti-prostatic Hypertrophic Action of Cernitin Pollen Extract (Cernilton ), Pharmacometrics, 31, 1986, 1-11. 8. Dutkiewicz S, Usefulness of Cernilton in the Treatment of Benign Prostatic Hyperplasia, International Urol and Nephrol, 28, 1996, 49-53. 9. Buck AC, et.al., Treatment of Outflow Tract Obstruction Ode to Benign Prostatic Hyperplasia with the Pollen Extract, Cernilton : A Double-blind, Placebo-controlled Study, Br J Urol, 66, 4, 1990, 398-404. 10. Habib ZX, et al. Isolation and characteristics of a cyclic hydroxamic acid from a pollen extract, which inhibits cancerous cell growth in vitro. J Med Chem.1994; 38 (4): 735-8
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Drug-Nutrient Interactions
Hormone Replacement Therapy and Oral Contraceptives Chaste Tree extract should be used with caution in patients taking these drugs. 18,20,22,23,24 5. L-Dopa, Levodopa, Haloperidol, Metoclopramide and other Dopamine Agonist Drugs Studies reveal that Chaste Tree extract may act in the body like some of these medications, which may alter the dose requirement of these drugs. As such, appropriate patient monitoring is required in these cases.25
4.
1. 2. 3. 4. 5.
Du Mee C. Vitex Agnus Castus. Australian Journal of Medical Herbalism 1993;5(3):63-5. Boon H, Smith M. The botanical pharmacy. Quarry Health Books 1998:76-81. Houghton P. Agnus Castus. The Pharmaceutical Journal 1994;253:720-1. Coeugniet E, Elek E, Kuhnast R. Premenstrual Syndrome (PMS) and its treatment. Arztezitchr Naturheilverf, 1986;27(9):61922. Dittmar F, Bohnert K, Peeters M. Premenstrual Syndrome: treatment with a phytopharmaceutical. Therapiewoche Gynakol 1992;5(1):60-8.
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6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25.
Loch E, Bohnert K, Peeters M. The treatment of menstrual disorders with Vitex Agnus Castus tincture. Der Frauenarzt 1991;32(8):867-70. Marie-Snow J. Vitex Agnus-Castus L. The Protocol Journal of Botanical Medicine 1996;1(4):20-3. Kubista E, Muller G, Spona J. Treatment of mastopathy with cyclic mastodynia, clinical results and hormone profiles. Gynakologische Rundschav 1986;26:65-79. Bleier W. Therapie von zyklus und blutungsstorungen und weiteren endokrin bedingten erkrankungen der frau mit pflanzlichen wirkstoffen. Zentralblatt Fur Gynakologie 1959;81(18):701-9. Propping D, Katzorke T, Belkein I. Diagnosis and therapy of corpus luteum defiociency in general practice. Therapiewoche 1988;38:2992-3001. Milewicz A, Gejdel E, Sworen H, et.al. Vitex Agnus-Castus extract in the treatment of luteal phase defects due to latent hyperprolactinemia: results of a randomised placebo-controlled double-blind study. Arzneimittelforschung 1993;43(7):752-6. Propping D, Katzorke T. Treatment of corpus luteum insufficiency. Zeitis Allgemeinmedizin 1987;63:932-3. Newall C, Anderson L, David Phillipson J. Herbal medicines: a guide for health-care professionals. London. The Pharmaceutical Press 1996:296. Bruckner C. In mitteleuropa genutze heilpflanzen mit milchsekretionsfordernder wirkung (galactagoga). Gleditschia 1989;17:189-210. Du Mee C. Vitex agnus castus. Australian Journal of Medical Herbalism 1993;5(3):63-5. Brown D. Vitex agnus castus clinical monograph. Quarterly Review of Natural Medicine 1994;2(2):111-21. Boon H, Smith M. Health care professional training program in complementary medicine. Institute of Applied Complementary Medicine Inc. 1997. Houghton P. Agnus castus. The Pharmaceutical Journal 1994;253:720-1. Murray M, Pizzarno J. Encyclopedia of natural medicine. Revised 2nd Edition. Prima Health 1998:750-1. Bohnert K. The use of vitex agnus castus for hyperprolactinemia. Quarterly Review of Natural Medicine. 1997;5(1):19-21. Merz P, Gorkow C, Schroder A, et al. The effects of a special agnus castus extract (BP1095el) of prolactin secretion in healthy male subjects. Endocrinology and Diabetes 1996; 104: 447-53. Milewicz A, et al. Vitex Agnus castus extract in the treatment of luteal phase defects due to latent hyperprolactinemia. Results of a randomized, placebo-controlled double-blind study. Arzneim Forsch/ Drug Res. 1993; 43 (7): 752-56. Amann W. Amenorrhea. Favorable effects of Agnus castus (Agnolyt) on amenorrhea. ZFA. (Stuttgart). 1082; 58 (4): 228-31. Sliutz G, etal. Agnus castus extracts inhibit prolactin secretion of rat pituitary cells. Hormone and Metabolic Research. 1993; 25: 253-55 Jarry H, et al. In vitro prolactin but not LH and FSH release is inhibited by compounds in extracts of Agnus castus: Direct evidence for a dopaminergic principle by the dopamine receptor assay. Exp Clin Endocrinol. 1994; 102 (6): 448-54
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Active Constituents
Primarily Flavonoids The flavonoid Baicalein within Chinese scullcap is considered to be its most important active constituent.3,5
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Anti-proliferative - Baicalein has also demonstrated anti-proliferative effects on human bladder cancer cell lines and a murine bladder cancer cell line, in vitro. In an in vivo experiment, mice were injected with bladder cancer cells with concurrent oral administration of a high baicalein-yielding supplement in one group, or with no baicalein supplementation in the control group. All the control mice showed a progressive increase in tumor volume over the ensuing days of the study, whereas the mice treated with baicalein (scutellaria) showed a significant inhibition of tumor growth.19 In other experiments, baicalein has demonstrated anti-proliferative effects on human pancreatic cancer cell lines and T lymphoid leukemia cells. The mechanism of action was shown to be through the reduction of protein tyrosine kinase activity and protein kinase C activity. Both of these enzyme activities are required for normal cellular proliferation to occur. Thus, in addition to inhibiting the 12 lipoxygenase enzyme pathway and inducing apoptosis of cancer cells, baicalein is also known to reduce cancer cell proliferation by directly or indirectly inhibiting specific enzymes (protein tyrosine kinase and protein kinase C) required for cellular division and proliferation.28 Antioxidant - Baicalein is also a strong antioxidant, and has been shown to protect DNA from undergoing cancerous mutations in challenge studies using potent carcinogens such as benzo{a}pyrene, and toxins such as aflatoxin (AF) B.1,20,21 Stimulates DNA repair enzymes - In vitro evidence indicates baicalein stimulates recombination and repair of damaged DNA, supporting its traditional inclusion in cancer formulas, and suggesting possible use after sunburn and radiation damage.22 Inhibits the 5alpha-reductase enzyme - Baicalein has been shown to inhibit the 5alpha-reductase enzyme, which converts testosterone to dihydrotestosterone (DHT). DHT is strongly associated with the development of prostate enlargement (benign prostatic hyperplasia) and prostate cancer. As such, baicalein is reported to be potentially useful for the prevention and/or treatment of androgen-dependent (testosterone-driven) disorders, including prostate enlargement and prostate cancer.23 Human Studies Involving Prostate Cancer Patients Studies on humans have primarily involved patients with advanced prostate cancer, who were shown to be unresponsive to traditional medical drugs and other interventions. In a study performed by researchers from the University of California at San Francisco and Memorial Sloan-Kettering Cancer Center in New York, the oral administration of a herbal combination containing baicalein to patients with metastatic prostate cancer (previously unresponsive to standard treatments) demonstrated reversal and/or stabilization of their condition with significantly improved survival, quality of life scores and other positive outcomes in almost all patients receiving the supplement. After a median treatment period of 57 weeks, 100% of patients with androgen-dependent cancer had a decline of 80% or more in their prostate-specific antigen (PSA) levels, and these levels were undetectable in 81% of the patients. In 31 of 32 patients, the testosterone level declined to that seen in castrated men. Of nine men with elevated prostatic acid phosphatase levels (a marker for cancer progression), all had declines of more than 50%. Of two patients with positive bone scans, one had a complete disappearance of cancerous bone lesions, and the other showed improvement. One patient had a complete disappearance of a bladder mass, demonstrated by CT scan. Of 35 patients with androgen-independent prostate cancer 54% showed a drop in their PSA levels by 50% or more, and of 25 patients with metastasis to bone, 2 showed marked improvement, 7 remained stable, 11 progressed, and 5 had no further bone scan follow up due to an increasing trend in their PSA levels.24 Other
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studies involving men with known prostate cancer, taking this herbal combination, have demonstrated similar results. In one study PSA levels dropped from 100ng/mL to 24 and from 386ng/mL to 114 within 16 months of supplementation in a two case report of hormone-refractory prostate cancer.25 Studies following larger groups of men with prostate cancer for up to four years have also shown this herbal formula to significantly reduce PSA levels and improve survival and quality of life scores.26,27 Researchers attribute much of the anti-tumor effects of this herbal combination to the presence of baicalein. According to researchers, baicalein has demonstrated impressive anti-cancer effects against androgendependent and androgen-independent human prostate cancer cells lines, and many of its anti-cancer mechanisms have been uncovered in recent years, in vitro and in vivo experiments.16,17,18,24,25,26,27,28 It appears to be of particular benefit in prostate cancer treatment and in combination with other phytonutrients (plant-based nutrients) and micronutrients (vitamins and minerals) may help to prevent the development of clinically important prostate cancer, reducing prostate cancer incidence.26 Animal studies indicate that baicalein may be effective in the treatment of other cancers as well, with experimental evidence supporting its potential use in stomach, pancreatic, bladder, liver12, 14, 15,19, 28 and breast cancer. 29, 30, 31 Hepatoma and Leukemia Patients Based on its traditional use, and the documentation of its anti-tumor effects against various human cancer cell lines, Baicalein has been used recently by doctors in Asia as a complementary supplemental agent in the treatment of hepatomas and leukemia in human subjects.29 2. Anti-viral/Anti-HIV Baicalein has been shown in experimental studies to inhibit the activity of HIV-1 integrase enzyme, which is an essential enzyme in the life cycle of the HIV-virus. This enzyme is responsible for catalyzing the insertion of the viral genome into the host cell chromosome. It is an attractive target for the design of a HIV antiviral drug because the integrase enzyme has no human counterpart.32 In a review of all herbal medicines frequently used as an alternative medical therapy by HIV positive patients and AIDS patients, JA Wu et al, emphasized that experimental data suggest that the flavonoid, Baicalein inhibits infectivity and replication of HIV, and shows great promise as an important component to be included in herbal remedies used for HIV treatment.33 3. Asthma and Allergies Baicalein inhibits type I and II hypersensitivity reactions, confirming its traditional use in asthma34,35 and allergic dermatitis.3 4. Anti-inflammatory Baicalein has shown impressive anti-inflammatory effects that appear to be mediated via repression of leukotriene B4 (inhibition of the 5-lipoxygenase enzyme), inhibition of interleukin-1B, and prostaglandin E2. Studies reveal it may be of benefit in the treatment of gingivitis (gum inflammation).29, 36, 37
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5. Alzheimers and Dementia In a rat model Baicalein has been shown to prevent the build up of amyloid beta peptide (Abeta), which is known to generate free radical damage to brain cells and participate to a significant degree in the development and progression of Alzheimers disease. Additionally, chronic inflammation occurs in Alzheimers pathogenesis and Baicalein was shown to inhibit the 12- lipoxygenase enzyme responsible for brain inflammation, to a large degree. When tested against other known 12-lipoxygenase inhibitor agents, only Baicalein was able to attenuate both nerve cell death (apoptosis) and over-expression of Abeta production. As such, Baicalein may help to prevent or forestall the development of Alzheimers disease by reducing the build up of the toxic brain protein, Abeta and inflammatory mediators, and preventing brain cell death, which has been shown to be triggered by the accumulation of Abeta in affected brain cells. 38 In studies using human neuroblastoma cells, the antioxidant properties of Baicalein were shown to inhibit free radical damage to these nerve cells induced by treatment with hydrogen peroxide (a powerful free radical generating agent). The researchers argue that oxidative (free radical) stress plays an important role in the development of neurodegenerative diseases (e.g. Alzheimers disease, Multiple Sclerosis, Parkinsons disease) and that antioxidants such as Baicalein and Quercetin (also a flavonoid) may be useful bioactive agents in the prevention and/or management of these conditions, pending further studies. Both of these flavonoids have shown impressive protective effects under experimental conditions.39 6. Inhibition of Xanthine Oxidase (Gout Treatment) Baicalein is one of few bioactive agents that has been shown to inhibit the enzyme xanthine oxidase, which is responsible for the conversion of hypoxanthine to xanthine, and xanthine to uric acid, in the pathway for degradation of purines in the body. High levels of uric acid is a hallmark feature of gout and thus, Baicalein supplementation may be an effective complementary intervention in the long-term management of this condition.40 The drug Allopurinol is a Xanthine Oxidase inhibitor and is a primary medication prescribed for the treatment of gout.
Dosage
Therapeutic Purposes: The usual doses for therapeutic purposes ranges from 150 to 200 mg per day of Baicalein.6 General wellness: Consider 50-100mg per day. Toxicity and Adverse Side Effects Baicalein supplementation at therapeutic doses appears to be safe with no reports of significant side effects or toxicity. Baicalein or Chinese scullcap are not known to be contraindicated for any health conditions.41,42
Drug-Nutrient Interaction
There are no known drug-nutrient interactions for Baicalein or Chinese skullcap.42
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Drug-Nutrient Interactions
Use with caution with patients on anti-asmathic and antihypertensive drugs, as forskolin may potentiate the effects of these drugs. As such, appropriate patient monitoring under these conditions is recommended .11,19
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1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.
Laurenza A, Sutkowski AM, Seamon KB. Forskolin: a specific stimulator of Adenylyl Cyclase or a Diterpene with multiple sites of action? Trends Pharmacol Sci 1989;10:442-7. Wong S, et.al. Forskolin inhibits platelet-activating factor binding to platelet receptors independently of Adenylyl Cyclase activation. Eur J Pharmacol 1993;245:55-61. Kramer W, et.al. Effects of Forskolin on left ventribular function in dilated Cardiomyopathy. Arzneimittel-Forsch 1987;37:364-7. Schlepper M, Thormann J, Mitrovic V. Cardiovascular effects of Forskolin and phosphodiesterase III inhibitors. Basic Res Cardiol 1989;84(Suppl 1):197-212. Wysman DG, Brotherton AF, Heistad DD. Effects of Forskolin on cerebral blood flow: implications for a role of adenylate cyclase. Stroke 1986;17:1299-1303. Lichey J, et.al. Effect of Forskolin on metacholine-induced bronchoconstruction in entrinsic asthmatics. Lancet 1984;ii:167. Allen DD and Quesenberry JT, Quantitative Differences in the Cyclic AMP-lipolysis Relationships for Isoproterenol and Forskolin, J Pharmacol Exp Ther 1988;244:862-858. Allen DO, Ahmed B, Naseer K. Relationship between cyclic AMP-levels and lipolysis in fat cells after isoprotenol and Forskolin stimulation. J Pharmacol Exp Ther 1986;238:659-64. Okuda H, Morimoto C, Tsujita T. Relationship between cyclic AMP production and lipolysis induced by Forskolin in rat fat cells. J Lipid Res 1992;33:225-31. Bianco AC, Kieffer JD, Silva JE. Adenosine 3, 5-monophosphate and thyroide hormone control of uncoupling protein messenger ribonucleic acid in freshly dispersed brown adipocytes. Endocrinology 1992;130:2625-33. Murray MT. The healing power of herbs. 2nd edition. Prima Publishing 1995. Gabetta B, et al. Minor diterpenoids of coleus forskohlii. Phytochemistry.1989;28(3):859-862. Natural Products Encyclopedia. www.consumerslab.com: Coleus Forskohlii. Palou A, et al.The uncoupling protein, thermogenin. Int J Biochem. Cell Biol. 1983;30(1):7-11. Murray MT. The unique pharmacology of coleus forskohlii. Health Counselor. 1995;7(2):33-35. Research Report, Sabinsa Corporation, 1999 Allen DO, et al. Relationships between cyclin AMP levels and lipolysis in fat cells after isoproterenol and forskolin stimulation. J Pharmacol and Exper Therap,1986;238(2):659-664 Haye B, et al. Chronic and acute effects of forskolin on isolated thyroid cell metabolism. Molecular and Cellular Endocrin. 1985;43:41-50. Dietary Supplement Information Bureau. www.content.intramedicine.com: Coleus Fosrkohlii
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Cranberry
General Features
Cranberry is an evergreen yielding shiny red berries and is native to the marshland of Northern Europe, Eastern Canada, and Eastern United States.1 It is a member of the same family as blueberry and bilberry. Its historical use as a treatment for bladder infections, originating with Native Americans, has recently been supported scientifically, and is the most well recognized application for Cranberry supplementation.1,4,6
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Drug-Nutrient Interactions
There are no reported drug-nutrient interactions for Cranberry , although weakly alkaline drugs may be affected, including antidepressants and prescription painkillers.1,17
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12. Sobota AE. Inhibition of bacterial adherence by cranberry juice: potential use for the treatment of urinary tract infection. Journal of Urology 1984;131:1013-6. 13. Zafriri D, Ofek I, Adar R, Pocino M, Sharon N. Inhibitory activity of cranberry juice on adherence of Type I and Type P fimbriated escherichia coli to eukaryotic cells. Antimicrobial Agents and Chemotherapy 1989;33(1):92-8. 14. Brown D. Herbal prescriptions for better health. Rocklin, CA. Prima Publishing 1996:349. 15. Howell AB, Vorse N, Der Maderosian a. Inhibition of the adheeence of P-fimbriated Escherichia coli to uroepithelial-all surfaces by proanthocyanidin extracts from cranberries. N Eng J Med.1998;339:1005-6. 16. Dietary Supplement Information Bureau. www.content.intramedicine.com: Cranberry. 17. Healthnotes, Inc.2001. www.healthnotes.com: Cranberry 18. Stothers LA. A randomized placebo controlled trial to evaluate naturopathic cranberry products as prophylaxis against urinary tract infection in women. Presented at: Am Urological Association 2001 Annual Meeting; June 2-7,2001; Anaheim, California. Publ ID:318
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Mechanism of Action
The mechanism of action is twofold. The active constituents: increase bile production and flow to the gallbladder (cholerectic effect) increase contraction of the gallbladder, releasing stored bile (cholagogue effect) to the intestinal tract. The high choline content of Dandelion root may also be an important aspect of Dandelions ability to influence bile flow.5
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Drug-Nutrient Interactions
Diuretic Drugs - do not use in conjunction with diuretic drugs, as Dandelion may potentiate the diuretic effect due to its high potassium content. 7,8
1.
Hobbs C. Taraxacum officinale: a monograph and literature review. In: Eclectic dispensatory. Portland: OR. Eclectic Medical Publications 1989. 2. Faber K. The dandelion taraxacum officinale. Pharmazie 1958;13:423-36. 3. Susnik F. Present state of knowledge of the medicinal plant taraxacum officinale weber. Med Razgledi 1982;21:323-8. 4. Bohm K. Choleretic action of some medicinal plants. Arzneimittel-Forsch 1959;9:276-378. 5. Murray M. The healing power of herbs. 2nd edition. Prima Publishing 1995:86-91. 6. Bradley P. British herbal compendium. Bournemouth. BHMA 1992:239. 7. Houghton P. Bearberry, dandelion, and celery. The Pharmaceutical Journal 1995;225:272-3. 8. Hirono I, et.al. Safety examination of some edible plants, part 2. Journal of Environmental Pathology Toxicology and Oncology 1977;1:72-4. 9. Healthnotes, Inc.2001. www.healthnotes.com: Dandelion. 10. Natural Products Encyclopedia. www.consumerslab.com: Dandelion
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Devils Claw
General Features
Devils Claw is a native plant of southern Africa. Its unusual name stems from the herbs fruits, which seem to be covered with numerous small hooks. The secondary storage roots, or tubers of the plant are used for medicinal purposes.1 Decoctions of dried roots have been taken as a tea by indigenous peoples for a variety of digestive and rheumatic conditions.2 It was introduced to Europe by Mehnert and became so popular that in 1976, it was estimated that 30,000 arthritis patients in the United Kingdom alone were using it.3
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Drug-Nutrient Interactions
Bleeding Disorders - Devils Claw has been shown to potentiate the anti-coagulant effects of warfarin and possibly the platelet inhibitor drug known as Ticlopidine, used to prevent stroke and to treat intermittent claudication and other conditions. In one patient Devils Claw was associated with purpura (bleeding under the skin) when taken concurrently with warfarin.17,18 Thus, Devils Claw should not be taken concurrently with anticoagulant drugs such as, warfarin, coumadin, and aspirin.17
1. 2. 3. 4. 5. 6.
Tyler VE. The honest herbal. 3rd ed. Binghamton, NY. Pharmaceutical Products Press 1993:111-2. Weiss R. Herbal medicine. Beaconsfield. Beaconsfield Press 1988:362. Grahame R, Robinson B. Devils Claw (Harpagophytum Procumbens): pharmacological and clinical studies. Ann Rheum Dis 1981;40:632. Boon H, Smith M. The botanical pharmacy. Quarry Health Books 2000:92-6. Bradley P. British herbal compendium. Bournemouth. BHMA 1992:239. Chevallier A. The encyclopedia of medicinal plants. London. Readers Digest 1996:336.
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7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.
Hoffman D. Holistic herbal. Rockport, MA. Element Books 1996:256. Soulimani R, Younos C, Mortier F, Derrieu D. The role of stomachal digestion on the pharmacological activity of plant extracts, using as an example of harpagophytum procumbens. Canadian Journal of Physiology and Pharmacology 1994;72(12):1532-6. Lanhers M, Fleurentin J, Mortier F, et.al. Anti-inflammatory and analgesic effects of an aqueous extract of harpagophytum procumbens. Planta Medica 1992;58:117-23. Newall C, Anderson L, David Phillipson J. Herbal medicines: a guide for health care professionals. London. The Pharmaceutical Press 1996:296. Whitehouse L, Znamirowska M, Paul C. Devils Claw (Harpagophytum Procumbens): no evidence for anti-inflammatory activity in the treatment of arthritic disease. Canadian Medical Association Journal 1983;129:249-51. Moussard C, Alber D, Toubin M, Thevenon N, Henry J. A drug used in traditional medicine, Harpagophytum Procumbens: no evidence for NSAID-like effect on whole blood eicosanoid production in humans. Prostaglandins Leukotrienes and Essential Fatty Acids 1992;46:283-6. Pinget M, Lecomte A. The effects of Harpagophytum Capsules (Arkocaps) in degenerative Rheumatology. Medecine Actuelle 1985;12:65-7. Chrubasik S, et.al. Effectiveness of Harpogophytum Procumbens in treatment of acute low back pain. Phytomed 1996;3:1-10. Whitehouse LW, et.al. Devils Claw (Harpagophytum Procumbens): no evidence for anti-inflammatory activity in the treatment of arthritic disease. Can Med Assoc J 1983;129:249-51. Grahame R, et.al. Devils Claw (Harpagophytum Procumbens): pharmacological and clinical studies. Ann Rheum Dis 1981;40:632. Healthnotes Online. Healthnotes, Inc. 2000. Shaw D, et al. Traditional remedies and food supplement: a 5-year toxicological study. Drug Safety 1997:17(1991-1995):342-56. Dietary Supplement Information Bureau. www.content.intramedicine.com: Devils claw.
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it has been tested as a preventive agent in this regard . 11 Thus, at this time Echinacea is not recommended as a supplement to be taken for long periods, but is rather used most effectively as a short-term intervention to rally the immune system during the early (prodromal) stages of an upper respiratory tract infection. 1,6,7 Best Variety: Some experts suggest that Echinacea Purpurea is the best variety because it provides the greatest range of active compounds and has the greatest level of clinical research support. 1
Other concerns are based upon the long-term administration of Echinacea and the possibility of over-stimulating the immune system in at risk individuals. As such, Echinacea should not be used by people with autoimmune disorders (Lupus, Rheumatoid Arthritis, etc.) and patients with multiple sclerosis, as there is evidence to show that it may trigger or aggravate such conditions. 15 A reported case also implicated the use of Echinacea in triggering recurrent episodes of erythema nodosum, an inflammatory condition that involves tender nodules under the skin. 16 As prolonged use of Echinacea may over-stimulate immune function and trigger underlying or hidden pathologies, the daily use of Echinacea for long periods as may occur in patients with impaired immune function (i.e., chronic fatigue), should not exceed eight weeks. The customary cycle of use in these cases is as follows: After one week of abstaining from Echinacea supplementation patients can begin another eight week cycle of supplementation, followed by one week off and so on.1 Thus, a primary concern of long-term use of Echinacea is rooted in the risk of sustained immune system enhancement, which may trigger some auto destructive consequences (i.e., attacking healthy body tissues, reawakening of dormant herpes viruses and/or, triggering autoimmune reactions). 1
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Drug-Nutrient Interactions
a. Immunosuppressive Drugs Echinacea counters the effects of these drugs and should not be used concurrently.17,18 b. Corticosteroid Medications Echinacea may counter the effects of these drugs in patients with autoimmune conditions and should not be taken concurrently.19
Murray MT. The Healing Power of Herbs. 2nd ed. Prima Publishing, 1995 Luetigg B, et.al. Macrophage activation by the polysaccharide arabinogalactan isolated from plant cell cultures of echinacea purpurea. J Nati Cancer Inst 1989;81:669-75. Tubaro A, et.al. Anti-inflammatory activity of a polysaccharide fraction of echinacea angustifolia root. J Pharm Pharmacol 1987;39:567-9. Roesier, J, et.al. Application of purified polysaccharides from cell cultures of the plant echinacea purpurea to mice medicates protection against systematic infections with listeria monocytogenes and candida albicans. Int J Immunopharmacol 1991;13:27-37. Brauning B, et.al. Echinacea purpurea radix for strengthening the immune response in flu-like infections. Z Phytother 1992;13:7-13. Healthnotes, Inc.2001.www.healthnotes.com: Echinacea. Dietary Supplement Information Bureau. www.content.intramedicine.com: Echinacea Duke JA. Handbook of phytochemical constituents of GRAS herbs and other economic plants. Boca Raton, FL: CRC Press, 1992. Melchart D, Linde K,Fisher P, et al. Echinacea for preventing and treating the common cold. Cochrane Database Syst Rev. 2000; (2): CDOOO530 Schulten B, Bulitta M, Ballering-Bruhl B, et al. Efficacy of Echinacea purpurea in patients with a common cold. A placebo-controlled, randomized, double-blind trial. Arzneimittelforschung. 2001; 51 (7): 563-8. Barrett B, Vohmann M, Calabrese C. Echinacea for upper respiratory infection. J Fam Pract. 1999; 48 (8): 628-35. Schultz V Hansel R, Tyler VE. Rational Phytotherapy: A Physicians Guide to Herbal Medicine. 3rd ed. Berlin, Germany: SpringerVerlag; 1998: 276 Parnham MJ. Benefit-risk assessment of the squeezed sap of the purple coneflower (Echinacea pupurea) for long-term oral immunostimulation. Phytomedicine. 1996; 3: 95-102.
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14. Mullins RJ, Heddle R. Adverse reactions associated with Echinacea: the Australian experience. Ann Allergy Asthma Immunol. 2002; 88: 42-51 15. Natural Products Encyclopedia. www.consumerslab.com: Echinacea. 16. Soon SL, Crawford RI. Recurrent erythema nodosum associated with Echinacea herbal therapy. J Am Acad Dermatol. 2001; 44:29899. 17. Vomel VT. Effect of a nonspecific immunostimulant on the phagocytosis of erythrocytes and the Ink by the reticulohistocyte-sytem in the isolated, perfused liver of rats of various ages. Arzneim Forsch/Drug Res. 1984; 34: 691-95 18. See DM, et al. In vitro effects of Echinacea and ginseng on natural killer and antibody-dependent cell cytotoxicity in healthy subjects and chronic fatigue syndrome or acquired immunodeficiency syndrome patients. Immunopharmacology. 1997; 35 (3): 229-35. 19. Bauer R. Echinacea Drugseffects and active ingredients. Z Arztl Fortbild. (Jena). 1996; 90 (2): 111-15.
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Ephedra
General Features
Various Ephedra species of plants are found throughout the world and grow in desert or arid regions. Ephedra sinica, also known as Ma Huang, is probably the best-known Ephedra species, but there are many others. They are erect, branching shrubs whose stems and branches contain alkaloids, of which 40-90 percent is the stimulant known as ephedrine and the remaining alkaloids being primarily pseudoephedrine and norpseudoephedrine. 1,2,3 Western medicines interest in Ephedra began in 1923, with the discovery that ephedrine possessed a number of pharmacological effects. Ephedrine was synthesized for pharmaceutical purposes in 1927 and since then both ephedrine and pseudoephedrine have been used extensively in over-the-counter cold and allergy medications.4 In 1973, more than 20 million prescriptions contained either ephedrine or pseudoephedrine.1
Increases blood pressure Increases cardiac output Increases heart rate Increases blood flow to the heart, brain, and skeletal muscle Decreases blood flow to the intestinal tract and kidneys Relaxation of bronchial muscles and uterine muscles 4
2.
Pseudoephedrine Pseudoeohedrine also relaxes bronchial muscles like Ephedra, but exerts weaker effects on the heart and central nervous system. Therefore, it is often recommended in the treatment of chronic asthma instead of ephedrine.4
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For weight loss patients, most of the studies have used a combination of 20 mg of ephedrine and 200 mg of caffeine, three times daily. Although significant weight loss results have been achieved using this approach (i.e., 36 lbs of weight loss in 24 weeks compared to 29 lbs in the placebo group), health practitioners and consumers should be aware of the dangerous side effects that can result (see Adverse Side Effects and Toxicity) from the use of ephedrine or Ephedra-containing supplements.7
Nervousness Insomnia Irritability Psychosis Headache Dizziness Seizures Stroke Premature ventricular contractions Increased blood pressure Myocardial infarction (heart attack) Sudden death 10,12,13
The Food and Drug Administration advisory review panel on non-prescription drugs recommended that ephedrine not be taken by patients with heart disease, high blood pressure, thyroid disease, diabetes, or difficulty in urination due to enlarged prostate or by patients taking antihypertensive or antidepressant drugs. 1 Other contra-indications include anxiety, glaucoma, pheochromocytoma.14
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Drug-Nutrient Interactions
Ephedra-containing products should not be used concurrently by patients taking the following medications:
Caffeine containing drugs Cardec DM Epinephrine containing drugs Nadolol Pheneizine Phenylpropanolamine 15 Monoamine oxidase inhibitors (MAO-inhibitors) Antidepressants Digoxin digitalis Antihypertensive drugs Guanethidine 16 Any Oral or Inhaled Anti-asthmatic medication 17,18
1. 2. 3. 4. 5. 6.
Murray M. The Healing Power of Herbs (2nd edition), Prima Publishing 1995:108-115 Chang HM and But PP. Pharmacology and Applications of Chinese Materia Medica, Vol.2, Teaneck, NJ: World Scientific Publishing, 1987 Duke JA. Handbook of Medicinal Herbs, Boca Raton, FL; CRC Press, 1985 Gilman AG, Goodman AS, and Gilman A. The Pharmacologic Basis of Therapeutics, New York: Macmillan, 1980 Lee T, et.al. Adrenomimetic Drugs in Craig C, Stitzel R, eds., Modern Pharmacology (4 th edition), New York;Little, Brown and Company 1994:907 Astrup A, et.al.. The Effect of Chronic Ephedrine Treatment on Substrate Utilization, the Sympatho-Adrenal Activity, and Expenditure During Glucose-induced Thermogenesis in Man, Metabolism 1986;35:260-265
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Astrup A, et.al.. Pharmacology of Thermogenic Drugs, AM J Clin Nutr 1992;55(1):246S-248S. Astrup A, et.al. The Effect and Safety of an Ephedrine / Caffeine Compound Compared with Ephedrine, Caffeine, and Placebo in Obese Subjects on an Energy Restricted Diet, Int J Obesity 1992;16:269-277 Dulloo AG, et.al. The Thermogenic Properties of Ephedrine / Methyxanthine Mixtures; Human Studies, Int J Obesity 1986;10:467481 Colgan M. Optimum Sports Nutrition, Advanced Research Press 1993, 454-455 McNeill JR, Interactions Between Herbal and Conventional medicines, Can J Cont Medical Educ 1999;11(12):97-110 Nightingale SL. From the Food and Drug Administration, JAMA 1996;275(20):p1534 Kikutani T. Contrary Views on Chinese Herbal Drugs and Side Effects, Int J Oriental Med 1990;15(4):184-188 Blumenthal M, et.al. The Complete German Commission E Monographs: Therapeutic Guide to Herbal medicine, Austin, Texas;American Botanical Council 1998:p685 Healthnotes Online, Healthnotes, Inc. 2000 Blumenthol M, et.al.(eds.) The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines, Boston, MA;Integrative Medicine Communication 1998:125-126 Faurshou M, et al. {The bronchodilating effect of ephedrine tablets in bronchial asthma}. Ugeskr Laeger 1993;155(46):3784-5 Laitinen LA, et al. A comparison of the bronchodilator action of pseudoephedrine and ephedrine in patients with reversible airway obstruction. Eur J Clin Pharmacol 1982;23(2):107-9
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Feverfew
General Features
Feverfew is a member of the sunflower family with the richest source of active constituents found within its leaves. The leaves of the plant contain a unique group of sesquiterpene lactones (85% of which is parthenoloide), which some studies suggest are its primary bioactive agent. Feverfew supplementation has demonstrated an ability to help reduce the frequency, and severity of migraine headaches is some individuals and this is its best-known therapeutic application for which it has gained immense popularity.6,8
A number of well-designed clinical trials have demonstrated that Feverfew supplementation can reduce the frequency of migraine headaches if taken on a preventive basis each day by migraine sufferers. The Nottingham trial involving 59 migraine patients showed a 24% reduction in number of migraine headaches in an eight-month placebo-controlled crossover trial. 4 The clinical studies by Palevitch et al, and Prusinki et al, also demonstrated success in reducing migraine frequency in human subjects with a strong history of migraine headaches. 8, 9 As noted above, a Dutch study reported no benefit from the use of a Feverfew extract over placebo tablets in migraine sufferers. 7 A recent review in the Cochrane Database Systematic Review, by Pittler et al, concludes that the majority of trials suggest a beneficial effect of Feverfew compared with placebo, but the efficacy of Feverfew for the prevention of migraine has not been established beyond a reasonable doubt. 10
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2. Rheumatoid arthritis Due to its anti-inflammatory effects, the traditional use of Feverfew has also included the management of rheumatoid arthritis. A double-blind study testing this application provided encouraging results, however this should be regarded as preliminary evidence only. 5
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a. Mammalian Lignan Precursors In particular: Secoisolariciresinol and matairesinol. These are converted into the mammalian lignans, enterolactone and enterodiol by colonic bacteria. Enterolactone and enterodiol are phytoestrogens and exhibit other functions (i.e. antioxidants). b. Alpha-Linolenic Acid (an Omega-3 fat) The amount of alpha-linolenic acid in Flaxseed Powder is far less than in flaxseed oil (see flaxseed oil, alphalinolenic acid), which is more likely to provide more significant health-promotion effects related to Omega-3 fat consumption (e.g., anti-inflammatory effects) c. Fiber Soluble and insoluble fiber 4,5,6
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Provide antioxidant protection 7 Lifetime exposure and gestational exposure to Flaxseed lignans induces cancer prevention structural changes to mammary glands and endocrine changes consistent with a reduced risk of breast cancer development in animals 12 Induce cancer cell differentiation Inhibition of tyrosine kinase and DNA topoisomerase two key enzymes that determine the rate of cell division 8 Anti-mitotic effect 4 Reduction of plasma insulin-like growth factor-1 levels (IGF-1) in rats. Higher IGF-1 blood levels is associated with an increased risk of breast cancer in some human studies 9 Reduction of pulmonary metastasis of melanoma cells and inhibit the growth of metastasic tumors that formed in the lungs of mice 10 Human Evidence - Enterolactone and enterodiol have been shown to exhibit the following anti-cancer functions in human studies: Antiproliferative effect on the breast, similar to that of other selective estrogen receptor modulators, such as tamoxifen and raloxifen 11 Stimulate production of sex hormone-binding globulin (SHBG), decreasing levels of free unbound sex hormones 12 Decrease the synthesis of 16-alpha hydroxyestrone and increase the synthesis of 2 hydroxyestrone. 13 A higher 2 hydroxyestrone to 16-alpha hydroxyestrone ratio (urinary metabolites) has been shown to be related to a decreased risk of breast cancer in women. This is a suggested chemoprotective effect. 14 Breast cancer patients excrete very low levels of lignans compared with non breast cancer subjects 4 Vegetarian women are known to have a lower incidence of breast cancer and exhibit higher blood levels of mammalian lignans 15 Improvement in cystic mastalgia, a potentially precancerous condition in women 16 Increased or longer luteal phase, increased progesterone to estradiol ratios during the luteal phase, fewer anovulatory cycles, and a decreased tendency to ovarian dysfunction; all of which are linked to a reduced risk of breast cancer in women 4 Cyclical Mastalgia In a double blind placebo-controlled study by Plu-Bureau et al, they demonstrated that patients ingesting the flaxseed muffin (25gm Flaxseed ) reported a significant improvement in breast pain reduction compared to the placebo group, during the three consecutive menstrual cycle duration of the trial. Results were attributed to the antiestrogen effects of Flaxseed lignans. 16
2.
3.
Cholesterol Lowering and Other Effects on Reducing Cardiovascular Disease Animal studies originally suggested that Flaxseed intake had a hypocholesterolemic effect, that is due to its soluble fiber concentration, not to its alpha-linolenic acid content.16 In human trials including men and postmenopausal women with high blood cholesterol levels, Flaxseed Powder or Flaxseed supplementation in various forms has been shown to reduce total cholesterol (approximately 7-10 percent), reduce LDL-cholesterol (approximately 15 percent), reduce lipoprotein (a) (Lp(a)) concentrations by approximately 7 percent. Lp(a) is emerging as an important risk factor for cardiovascular disease as it increases
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clotting behaviour of platelets, cholesterol deposition in the artery wall and it oxidizes LDL-cholesterol, making it very atherogenic. Flaxseed supplementation is the only dietary factor shown to reduce Lp(a) to date. Estrogen replacement therapy reduces Lp(a) levels, but cholesterol lowering drugs (i.e. statin drugs) do not 17,18,19 Flaxseed lignans inhibit the cholesterol-7-alpha hydroxylase and acyl CoA cholesterol transferase enzymes, involved in cholesterol synthesis, thus reducing total cholesterol. 24 1. Chronic Renal Failure and Renal Disease In Lupus Animal and human studies indicate that a diet rich in soy based protein and isoflavones, and/or Flaxseed lignans retard the development and progression of chronic renal disease. The protective effect is considered to be due to effects on cell growth and proliferation, extracellular matrix synthesis, reduced oxidative stress and inflammation reduction 20 In humans (and animals) Flaxseed supplementation has demonstrated renoprotective effects in human lupus nephritis, with significant delay in the onset of proteinuria, and preservation of the glomerular filtration rate (GFR) and renal size 5. Bone Density and Menopausal Symptom Support Preliminary evidence in women suggests that the phytoestrogen influence of enterolactone and enterodiol (from Flaxseed supplementation) has a positive effect on bone density and menopausal symptoms (i.e. hot flashes) 11 6. Prostate Cancer Protective Effect Flaxseed lignans interfere with steroid metabolism and bioavailablity in a fashion that is linked to reduced prostate cancer risk. They also inhibit enzymes such as tyrosine kinase and topoisomerase, which initiate the cellular proliferation rate. Epidemiological studies link the above endocrine and molecular events with up to an 80 percent reduction in risk of prostate cancer 22 7. Constipation Human studies reveal that Flaxseed supplementation improves laxation 5 It appears that Flaxseed intake increases fecal excretion of bile acids, increasing laxation and reducing the conversion of bile acids to cholesterol in the liver; thereby lowering blood cholesterol 23,5
Dosage Ranges
1. 2. 3. General Health and Cholesterol Lowering: 2550 gms of ground flaxseeds per day (unground seeds are significantly less bioavailable in regards to their lignan precursors content) 1, 13,14,17,18,19 Cyclical Mastalgia: 25 gm per day of ground Flaxseed Powder1,13,14,16 Female Menopausal Support: 25-50 gm per day of ground Flaxseed Powder13,14
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xx. xxi. xxii. xxiii. xxiv. xxv. xxvi. xxvii. xxviii. xxix.
Gross PE et al. Effect of dietary flaxseed in women with cyclical mastalgia. Program and abstract of the 23rd Annual San Antonio Breast Cancer Symposium. Dec 6-9 2000; San Antonio Texas. Abstract 153. Breast Cancer Res Treat. 2000;64:49 Arjmandi BH et al. Whole flaxseed consumption lowers serum LDL-cholesterol and lipoprotein (a) concentrations in postmenopausal women. Nutr Res 1998;18:1203-14 Jenkins DJA et al. Health aspects of partially defatted flaxseed, including effects on serum lipis, oxidative measures, and ex vivo androgen and progestin activity : a controlled cross over trial. Am J Clin Nutr 1999;69(3):395-402 Flaxseed Lowers Cholesterol. Nutr Science News 1998;3(11):575 Velasquez M et al. Dietary Phytoestrogens : A possible role in renal disease prtection. Am J Kidney Dis 2001;37(5):1056-68 Clark WF et al. A novel treatment for lupus nephritis : lignan precursor derived from flaxseed. Lupus 2000;9(6):429-36 Denis L et al. Diet and its preventive role in prostate disease. Eur Urol 1999;35(5-6):377-87 Chen WJL et al. Hypocholesterolemic effects of soluble fibers. In Kritchevsky D, Yahouny GD, eds. Dietary Fiber: basic and clinical aspects. New York: Plenum Press, 1986:275-89 Sanghui A et al. Inhibition of rat liver cholesterol 7-alha hydroxylase and acyl CoA : cholesterol acyl transferase activities by enterodiol an enterolactone. In Kritchevsky D, ed. Proceedings of the Symposium on Drugs Affecting Lipid Metabolism. New York: Plenum Press, 1984:311-322 Healthnotes Online. Healthnotes Inc. 2000. www.healthnotes.com: Flaxseed
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1. The quantity of S-allyl cysteine (SAC) present in various Garlic preparations has been shown to correlate with the ability of these preparations to inhibit in-vivo formation of DNA adducts resulting from DMBA treatment. Other nutrients enhance the protective effects of Garlic in cancer studies. These nutrients include selenium and vitamin A. The pungent odor of Garlic is caused mainly by allicin. Allinase enzyme within Garlic converts alliin into allicin upon damage or crushing of Garlic cells. The crushing process brings allinase enzyme into contact with alliin allowing this reaction to occur. Thus, S-allyl-L-cysteine sulphoxide (alliin) decomposes into the reactive intermediate allyl sulphenic acid, two molecules of which spontaneously condense to form diallyl thiosulphinate (allicin). Allicin compromises 6575% of the total thiosulphate concentration of Garlic preparations.2,3,4,5,6,7,8,9,10,11,12,13,14,15 2. Cardiovascular Studies Studies reveal that Garlic has a beneficial effect on blood lipids, blood pressure, blood coagulation, and LDL oxidation. In one study, 432 individuals who had suffered a heart attack were given either Garlic oil extract or no treatment over a period of 3 years. The results showed a significant reduction of second heart attacks and about a 50% reduction in death rate among those taking Garlic.42 Mechanisms: Lowering of total cholesterol by 10-12% or by 9%, on average (meta-analysis of controlled studies Warshafsky S) has been established, with the equivalent of one-half clove Garlic daily, delivering 4,000 mcg of allicin. Garlic compounds may block absorption of cholesterol or the re-absorption of bile from the gut, or inhibit the action of HMG CoA reductase enzyme, according to experimental studies. All of these biological actions would produce a decline in blood cholesterol levels. Garlic may also raise HDL-cholesterol levels. Lowering of blood pressure in hypertensive patients by 20-30 mm Hg systolic pressure and 10-20 mm Hg diastolic pressure (study by Foushee OB) has also been demonstrated. However, it is not clear at this time if Garlic supplementation can consistently help to lower blood pressure to any appreciable degree. Decreased platelet stickiness Ajoene, a self-condensation product, is as potent as aspirin as an anti-coagulant agent, and its activity is enhanced by two breakdown products which are also present in Garlic. (Rose KO, et.al. Neurosurgery 26:880-882, 1990). Garlic also increases fibronolytic activity significantly, dissolving blood clots (Chutani SK and Legnani C) and improving blood flow. Decreased LDL oxidation 600 mg per day of a Garlic preparation yielding 7.8 mg of alliin for two weeks reduced LDL-oxidation by 34 percent compared to controls. (Phelps S, et.al.)16,17,18,19,20,21,22 Reduced LDL-cholesterol oxidation is associated with a lower risk of developing atherosclerosis and heart disease. 3. Antimicrobial Activity Garlic has been shown to have significant antibacterial, antifungal, anti-helmintic (anti-parasite) and antiviral properties, however, it should not be used as a replacement for antimicrobial or anti-parasite medications.23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39 One intervention trial did show that taking Garlic each day during the winter months reduced the frequency of colds (upper respiratory tract infections) by two-thirds compared to those receiving the placebo.43
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Drug-Nutrient Interactions
Anticoagulant Medications (e.g., Aspirin, Coumadin, Warfarin, Heparin, Plavix Ticlid and Trental): Garlic preparations are known to potentiate the effects of these drugs and may lead to a bleeding disorder and thus, Garlic products should not be combined with these drugs, without the attending physicians consent and proper monitoring of prothrombin time (INR). 47,48 Saquinavir: Garlic may decrease blood levels of this drug, thus altering the activity and dose requirement for this drug.
49
Garlic preparations may also potentiate the effects of hypolipidemic and antihypertensive medications, helping to lower the dose requirement and side effects of these drugs. 50,51,52
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17. Block E, et.al., Journal of the American Chemical Society 106, 1984, 8295-8296. 18. Rose KO, et.al., Neurosurgery 26, 1990, 880-882. 19. Foushee DB, Ruffin J and Baberjee U, Garlic as a Natural Agent for the Treatment of Hypertension: A Preliminary Report, Cytobios 34, 1982, 145-162. 20. Chutani SK and Bordia A, The Effect of Fried Versus Raw Garlic on Fibrinolytic Activity in Man, Atherosclerosis 38, 1981, 417-421. 21. Legnani C, et.al., Effects of Dried Garlic Preparation on Fibrinolysis and Platelet Aggregation in Healthy Subjects, ArzneimittelForsch 43, 1993, 119-121. 22. Phelps S and Harris WS, Garlic Supplementation and Lipoprotein Oxidation Susceptibility, Lipids 28, 1993, 475-477. 23. Adetumbi MA and Lau BH, Allium Satibum (garlic) A Natural Antibiotic, Med Hypothesis 12, 1983, 227-237. 24. Koch HP, Garlicin Fact or Fiction?, Phytother Res 7, 1993, 278-280. 25. Hughes BG and Lawson L, Antimicrobial Effects of Allium Sativum L (Garlic), Allium Ampeloprasum L (Elephant Garlic) and Allium, Cepa L (Onion), Garlic Compounds and Commercial Garlic Supplement Products, Physiother Res 5, 1991, 154-158. 26. Huddleson IF, et.al., Antibacterial Substances in Plants, J Am Vet Med Assoc 105, 1944, 394-397. 27. Cavallito CJ and Bailey JH, Allicin, the Antibacterial Principle of Allium Sativum, I Isolation, Physical Properties and Antibacterial Action, J Am Chem Soc 66, 1944, 1950-1951. 28. Sharma VD, et.al., Antibacterial Property of Allium Sativum Linn: In Vivo and In Vitro Studies, Indian J Exp Biol 15, 1977, 466-468. 29. Elnima El, et.al., The Antimicrobial Activity of Garlic and Onion Extracts, Pharmazie 38, 1983, 747-748. 30. Amer M, Taha M, And Tosson Z, The Effect of Aquenous Garlic Extract on the Growth of Dermatophytes, Int J Dermatol 19, 1980, 285-287. 31. Moore GS and Atkins RD, The Fungicidal and Fungistatic Effects of an Aqueous Garlic Extract on Medically Important Yeast-like Fungi, Mycologia 69, 1977, 341-348. 32. Sandhu DK, Warraich MK, and Singh S, Sensitivity of Yeasts Isolated from Cases of Vaginitis to Aqueous Extracts of Garlic, Mykosen 23, 1980, 691-698. 33. Prasad G and Sharma VD, Efficacy of Garlic (Allium Sativum) Treatment Against Experimental Candidiasis in Chicks, Br Vet J 136, 1980, 448-451. 34. Hunan Hospital, Garlic in Cryptococcal Meningitis: A Preliminary Report of 21 Cases, Chin Med J 93, 1980, 123-126. 35. Fromtling R and Bulmer G, In Vitro Effect of Aqueous Extract of Garlic (Allium Sativum) on the Growth and Viability of Cryptococcus Neoformans, Mycologia 70, 1978, 297-405. 36. Vahora SB, Rizwan M, and Khan JA, Medical Uses of Common Indian Vegetables, Planta Medica 23, 1973, 281-393. 37. Bastidas GJ, Effect of Ingested Garlic on Necator Americanus and Ancylostoma Canium, Am J Trop Med Hyg 18, 1969, 920-923. 38. Nagai K, Experimental Studies on the Preventive Effect of Garlic Extract Against Infection with Influenza Virus, Jpn J Infec Dis 47, 1973, 321. 39. Wever ND, et.al., In Vitro Virucidal Effects of Allium Sativum (Garlic) Extract and Compounds, Planta Medica 58, 1992, 417-423. 40. Murray MT, The Healing Power of Herbs (2nd edition), Prima Publishing, 1995. 41. Natural Products Encyclopedia. www.consumerslab.com: Garlic 42. Bordia A. Garlic and coronary heart disease. The effects of garlic extract therapy over three years on the reinfarction and mortality rate. Dtsch Apoth Ztg. 1989; 129 (suppl 15): 16-17. 43. Josling P. Preventing the common cold with a garlic supplement: a double-blind, placebo-controlled survey. Adv Ther. 2001; 18 (4): 189-193. 44. Healthnotes, Inc.2001 www.healthnotes.com: Garlic. 45. Natuarl Products Encyclopedia. www.consumerslab.com: Garlic. 46. McNeill JR. Interactions between herbal and conventional medicines. Can J CME. 1993; 11 (12): 97-110 47. Kiesewetter H et al. Effect of garlic on platelet aggregation in patients with increased risk of Juvenile Ischaemic Attack. Eur J Clin Pharmacol 1993;45(4):333-6 48. Rose KD, Croissant PD, Parliament CF, Levin MB. Spontaneous spinal epidural hematoma with associated platelet dysfunction from excessive garlic ingestion: a case report. Neurosurgery. May 1990;26(5):880-2 49. Piscitelli SC, Bursein AH, Welen N, Gallicano KD, Falloon J. The effect of garlic supplements on the pharmacokinetics of saquinavir. Clinical Infectious Diseases. Jan 15 2002;34. Published on line Dec 5 2001. Accessed at: http://www.journals.uchicago.edu/CID/journal/issues/v34n2/010586.abstract.html 50. Steiner M et al. A double-blind crossover study in moderately hypercholesterolemic men that compared the effect of aged garlic extract and placebo administraion on blood lipids. Am J Clin Nutr 1996;64(6):866-70 51. Koscielny J et al. The antiatherosclerotic effect of allium sativum. Atherosclerosis May 1999;144(1):237-49 52. Fogarty M. Garlics potential role in reducing heart disease. Br J Clin Pract 1993;47(2):64-5
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Ginger
General Features
Ginger is native to southern Asia and has been used as food and medicine in many areas of the world for millennia. 16 The knotted and branched rhizome, commonly called the root is the portion of Ginger used for culinary and medicinal purposes. 1,13,16 Gingers modern day use dates back to the early 1980s when a scientist named D. Mowrey noticed that the Ginger-filled capsules reduced his nausea during an episode of flu. 16
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2. Anti-inflammatory Effects in Arthritis Ginger has been shown to posses anti-inflammatory properties and has been effective in several small studies to control pain and inflammation in patients with a variety of arthritic and musculoskeletal inflammatory conditions. 10,26 Experimental investigations suggest that Ginger inhibits the synthesis of pro-inflammatory prostaglandins, by inhibiting both the cyclo-oxygenase and 5-lipoxygenase enzymes. 7,8,9,10 It also has antioxidant properties and contains protease enzymes, which may add to its anti-inflammatory properties. 13 In a study of 56 patients (28 with rheumatoid arthritis, 18 with osteoarthritis and10 with muscular discomfort), Ginger supplementation was effective in reducing pain and inflammation in three-quarters of the arthritis patients and all of the patients with muscular discomfort. No adverse side effects were reported in these patients who were followed for up to 2.5 years. 10 Experimental evidence is strong to illustrate the anti-inflammatory activities of Ginger. 1,2,3,4,5 An interesting side note is that in contrast to anti-inflammatory drugs (aspirin, ibuprofen, COX-2 inhibitors and other non steroidal anti-inflammatory medications) that are known to cause erosion and ulceration (sometimes internal bleeding) of the intestinal tract, Ginger has been shown to protect the stomach from the damaging effects of alcohol, non steroidal anti-inflammatory drugs and, may help prevent peptic ulcers. 27 3. Migraines Ginger may also help to prevent the recurrence of migraines due to its anti-inflammatory and anti-platelet aggregation properties.1 However, greater substantial evidence exists for the herb feverfew as a daily preventive supplement for migraine prevention (see Feverfew in this document).
2. Arthritis and Musculoskeletal Inflammatory Conditions: Studies show that if used as a sole anti-inflammatory intervention that the daily dosage can range from 1,000 mg to 4,000 mg per day, based upon the dose required to reduce symptoms. 13,26
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Drug-Nutrient Interactions
Anticoagulant Medications (e.g., Aspirin, warfarin, coumadin, heparin, Plavix, Ticlid, Trental): As test tube experiments show that Ginger may reduce platelet clotting it may potentiate the activity of anticoagulant drugs, although no evidence of an anti-clotting effect for Ginger has been found in humans. Nevertheless, the patients prothrombin time (INR) should be monitored if Ginger is to be taken concurrently with any anti-coagulant drug, to guard against a potential bleeding disorder. 30,31,32
Boon H and Smith M, Health Care Professional Training Program in Complementary Medicine, Institute of Applied Complementary Medicine Inc., 1997. Mowrey D and Clayson D, Motion Sickness, Ginger, and Psychophysics, Lancet I, 1982, 655-657. Stewart JJ, et.al., Effects of ginger on Motion Sickness Susceptibility and Gastric Function, Pharmacology 42, 1991, 111-120. Grontved A, et.al., Ginger Root Against Seasickness A Controlled Trial on the Open Sea, Acta Otalaryngol 105, 1988, 45-49. Fischer-Rasmussen W, et.al., Ginger Treatment of Hyperemesis Gravidarum, Eur J Obstet Gynecol Reprod Biol 38, 1990, 19-24. Bone ME, et.al., Ginger Root-a New Antiemetic: The Effect of Ginger Root on Postoperative nausea and Vomiting After Major Gynecological Surgery, Anaesthesia 45, 1990, 669-671. Kiuchi F, et.al., Inhibition of Prostaglandin and Leukotriene Biosynthesis by Gingerols and Diaryheptanoids, Chem Pharm Bull 40, 1992, 387-391. Kuichi F, Shibuyu M, and Sankawa U, Inhibitors of Prostaglandin Biosyntheses from Ginger, Chem Pharm Bull 30, 1982, 754-757. Srivastava KC, Isolation and Effects of Some Ginger Components on Platelet Aggregation and Eicosanoid Biosyntheses, Prostaglandin Leurotrienes Med 25, 1986, 187-198. Srivastava KC and Mustafa T, Ginger (Zingiber Officinale) and Rheumatice Disorders, Med Hypotheses 39, 1992, 342-348. Srivastava KC and Mustafa T, Ginger (Zingiber Officinale) in Rheumatism and Muscoloskeltel Disorders, Med Hypotheses 39, 1992, 342-348. Mustafa T and Srivastava KC, Ginger (Zingiber Officinale) in Migraine Headaches, J Ethnopharmacol 29, 1990, 267-273. Murray MT, The Healing Power of Herbs (2nd edition), Prima Publishing, 1995.
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14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32.
Healthnotes, Inc.2001 www.healthnotes.com: Ginger Dietary Supplement Information Bureau. www.content.intramedicine.com: Ginger Natural Products Encyclopedia. www.consumerslab.com: Ginger Tyler VE. Herbs of Choice: the Therapeutic Use of Phytomedicinals. Binghampton, NY: Pharaceutical Products Press 1994: 39-42 Holtmann S, Clarke AH, Scherer H, Hohn M. The anti-motion sickness mechanism of ginger. A comparative study with placebo and dimenhydrinate. Acta Otolaryngol (Stockh) 1989;108:168-74 Holtmann S, Clarke AH, Scherer H et al. The anti-motion sickness mechanism of ginger. Acta Otolaryngol 1989;108:168-74 Bradley PR (ed.). British Herbal Compendium, vol 1. Bournemouth, Dorset, UK: British Herbal Medicine Association, 1992:112-4 Schmid R, Schick T, Steffen R et al. Comparison of seven commonly used agents for prophylaxis of seasickness. J Travel Med 1994;1:203-6 Riebenfeld D, Borzone L. Ranomized double-blind study comparing ginger (ZintonaW) and dimenhydrinate in motion sickness. Healthnotes Rev 1999;6:98-101 Tyler VE. Herbs of Choice: The Therapeutic Use of Phytomedicinals. New York, NY: Pharmaceutical Products Press; 1994:p42 Phillips S, Hutchinson S, Ruggier R. Zingiber officinale (ginger) An antiemetic for day case surgery. Anaesthesia 1993;48:715-7 Meyer K, Schwartz J, Craer D, Keyes B. Zingiber officinale (ginger) used to prevent 8-Mop associated nausea. Dermatol Nursing 1995;7:242-4 Srivastava KC, Mustafa T. Ginger (Zingiver officinale) in rheymatism and musculoskeletal disorders. Med hypotheses December 1992;39(4):342-8 al-Yahya MA, Rafatullah S, Mossa JS et al. Gastroprotective activity of finger in albino rats. Am J Chinese Med 1989;17:51-6 Srivastava KC. Effects of aqueous extracts of onion, garlic and ginger on platelet aggreagation and metabolism of arachidonic acid in the blood vascular system: in vitro study. Prostaglandins Leukoit Med 1984;13:227-35 Srivastava KC. Effect of onion and ginger consumption on platelet thromboxane production in humans. Prostaglandins Leukot Essent Fatty Acids 1989;35:183-5 Suekawa M et al. Pharmacological studies on Ginger. I. Pharmacological actions of pungent constitutents, (6)-gingerol and (6)shogaol. J Pharmacobiodyn 1984;7(11):836-48 Guh JH et al. Antiplatelet effect of gingerol isolated from zingiber officinalte. J Pharm Pharmacol 1995;47(4):329-32 Bordia A, Verma SK, Srivastava KC. Effect of ginger (Zingiber officinale Rosc.) and fenugreek (Trigonella foenumgraecum L.) on blood lipids, blood sugar and platelet aggregation in patient swith coronary artery disease. Prostaglandins Leukot Essent Fatty Acids. May 1997;56(5):379-84
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Ginkgo Biloba
General Features
Ginkgo Biloba is a deciduous tree that lives as long as 1,000 years and may grow to a height of 100-122 feet. Extracts from the leaves are used medicinally.1 It is the worlds oldest living tree species, traceable back 300 million years.1,38 Presently, ginkgo is the most wisely prescribed herb in Germany, reaching a total prescription count of over 6 million in 1995. German physicians consider it to be as effective as any other drug treatment for Alzheimers disease and other severe forms of memory and mental function decline. 38 Principle Active Constituents Ginkgo flavones Ginkgolides and bilobalide terpene molecules unique to ginkgo. Ginkgo Biloba extract is standardized to contain 24 percent flavonoid glycosides, as these molecules represent a convenient analytical reference group. The three major back bone flavonoids include: Quercetin Kaempferol Isorhamnetine It also contains other flavonoid components such as proanthocyanidins. The ginkgolides and bilobalides account for 6% of Ginkgo Biloba Extract.1,2
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2. Prevention of Memory Loss and Enhanced Memory in Healthy Subjects Several recent studies have evaluated the ability of ginkgo to prevent age-related memory loss, and to enhance the memory of otherwise healthy young subjects. A 30 day double-blind placebo-controlled study, following 50 healthy men and women (18 40 years of age ), demonstrated that 120 mg per day of Ginkgo Biloba Extract resulted in significant improvement in some measures of memory function. A double-blind study of 26 subjects found that a single dose of 120 mg of Ginkgo Biloba Extract improved short-term memory, especially in people over 50 years of age. In a double-blind placebo-controlled crossover trial involving 20 individuals aged 19 24 years, a one time dose of Ginkgo Biloba Extract at 120, 240, or 360 mg resulted in improvement of mental-performance, most dramatically in one test that measured ability to rapidly perform attention-related tasks. A smaller trial involving eight subjects (25 40 years of age) found some improvement in short-term memory with a single dosing of Ginkgo Biloba Extract at 60 mg, but not at lower levels of intake. However, not all studies with younger patients have shown an improvement in memory function and larger, more long-term trials are required before Ginkgo can be recommended with confidence for this application. 38 Mechanism of Action Experimental evidence has suggested that the active constituents in Ginkgo Biloba are able to improve memory and other aspects of cognitive function via the following actions: Decreased Platelet Aggregation Due to its antioxidant effects, increased synthesis of prostacyclin and antagonism of platelet-activating factor (PAF), Ginkgo Biloba Extract has been shown to improve blood flow to deeper centers of the brain, allowing a greater concentration of nutrients to reach these brain cells. This appears to have important considerations in cases of cognitive impairment due to cerebral vascular insufficiency. Decreased Lipid Peroxidation of Cellular Membranes of Red Blood Cells (which carry oxygen) and Nerve Cells (enhancing depolarization capacity and transmission of impulses) - Brain cells contain the highest percentage of unsaturated fatty acids in their membranes than any other cells in the body. This makes them extremely susceptible to free radical damage as unsaturated fatty acids contain double bonds, which are easily broken by free radicals in search of an electron. Ginkgo Biloba Extract, through its antioxidant capabilities, has been shown to prevent free radical damage to these structures, blocking lipid peroxidation and preserving the integrity of nerve cell membranes. This may help preserve or improve the transmission of nerve impulses from one nerve cell to the next, enabling better communication to occur among brain cells. Improves Synthesis and Turnover of Brain Neurotransmitters, and Normalizes Acetylcholine Receptors in the Hippocampus (the area of the brain most affected by Alzheimers disease) Evidence exists to show that Ginkgo Biloba Extract can enhance the synthesis of the memory chemical acetylcholine, and improve its ability to relay important chemical signals to other nerve cells in key areas of the brain that are affected in Alzheimers disease, and ARCD. Vasodilation Action Ginkgo Biloba Extract has been shown to cause the release of endothelium-derived relaxing factor (EDRF) and prostacyclin (a beneficial prostaglandin). The release of these bioactive agents within the body results in increased blood circulation and nutrient delivery to brain cells. 3 - 21 Direct Stimulation of Nerve Cell Activity Recent evidence suggests that like other drugs used for the treatment of dementia, Ginkgo Biloba Extract appears to directly stimulate nerve cell activity and in various ways protects nerve cells from further injury. 38
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1. Senile Macular Degeneration and Diabetic Retinopathy Preliminary studies indicate that Ginkgo Biloba Extract may be beneficial in the management of macular degeneration and diabetic retinopathy. 22, 38 Ginkgos antioxidant properties and its ability to improve blood flow through the tiny blood vessels in the macular region of the eye, may be of value in preserving vision in these patients. 22 Other synergistic nutrients for this condition include the antioxidants, Vitamin E, Vitamin C, Beta-carotene and zinc, the herbal agent bilberry, and the accessory nutrient grape seed extract (see details in related sections of this document). 2. Peripheral Artery Insufficiency (i.e., intermittent claudication due to atherosclerosis) Due to its ability to improve microcirculation, Ginkgo Biloba Extract has been shown to improve blood flow, and reduce pain (pain-free walking distance), in at least 10 studies involving patients with peripheral vascular insufficiency. 23 A review the American Journal of Medicine (2000) indicates that eight double-blind placebo-controlled trials, provide evidence that Ginkgo can significantly increase pain-free walking distance in these patients. 38 3. Altitude Sickness Exposure to high altitudes and cold conditions can cause vertigo, insomnia, shortness of breath, headache, as well as pain and numbness in the extremities. A single double-blind study of 44 mountain climbers demonstrated that 160 mg per day of Ginkgo Biloba Extract helped prevent many of these symptoms upon expedition in the Himalayan mountain range. 38 4. Vertigo (dizziness) 70 patients suffering from vertigo were given 160 mg of Ginkgo Biloba Extract daily or a placebo for three consecutive months. Results showed that the group given Ginkgo had a 47% recovery rate as compared to 18% in the placebo group. 38 5. Premenstrual Syndrome A single study showed that 160 mg of Ginkgo Biloba significantly reduced major symptoms of PMS, especially breast pain and emotional disturbances, compared to placebo, in a two-month trial involving 143 women, who were 1845 years of age. 38 6. Male Impotence Due to its ability to increase microcirculation of peripheral blood vessels Ginkgo Biloba Extract has been use successfully in a number of small trials as a treatment for male impotence resulting from impaired blood flow (e.g., diabetes and atherosclerosis). 29 It may also reveres the side effects of male impotence and failure to reach orgasm, associated with the use of certain antidepressant drugs, such as selective serotonin reuptake inhibitors (SSRI), according to one preliminary trial. 38
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Drug-Nutrient Interactions
1. Anticoagulants Ginkgo is known to potentiate the effects of anticoagulant drugs and bleeding disorders in the brain and cranial vault have been reported in humans. As such, Ginkgo should not be taken concurrently with anticoagulants, including aspirin, coumadin, warfarin, plavix, ticlid, trental etc. 32,33,34,35,38 2. Non Steroidal Anti-Inflammatory Drugs (NSIADs) Ginkgo may increase the risk of bleeding disorders associated with the use of NSAIDs, and thus should not be taken concurrently with these medications. 36 3. Monoamine Oxidase Inhibitors ( MAO- inhibitors) Ginkgo may potentiate the action of MAO-inhibitor antidepressant drugs, and thus should not be taken concurrently with these medications. 37
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DeFeudis FV (ed.), Ginkgo Biloba Extract (Egb 761): Pharmacological Activities and Clinical Application, Elsevier, Paris, 1991. Funfgeld EW (ed.), Rokan (Ginkgo Biloba): Recent Results in Pharmacology and Clinic, Sringer Verlag, NY, 1988 Kleijenen J, Knipshcild P. Ginkgo Biloba. Lancet 1992;340:1136-9 Kleijenen J, Knipschild P. Ginkgo Biloba for cerebral insufficiency. Br J Clin Pharmacol 1992;34:352-8 Schaeffler VK, Reeh PW. Double-blind study of the hypoxia-protective effect of a standardized ginkgo biloba preparation after repeated administration in healthy volunteers. Arzneimittel-Forsch 1985;35:1283-6 Chatterjee SS, Gabard B. Studies on the mechanism of action of an extract of ginkgo Biloba, A drug for the treatment of ischemic vascular diseases. Naunyn-Schmiedebergs Arch Pharmacol 1982;320(R52) Le Poncin et al. Effect of ginkgo biloba on changes induced by quantitative cerebral microembolization in rats. Arch Int Pharmacodyn Ther 1980;243:-44 Karcher L, Zagerman P, Kriedlstein J. Effect of a n extract of ginkgo biloba on rat brain energy metabolism in hypoxia. NaunynSchmiedebergs Arch Pharmacol 1984;327:31-5 Koltai M et al. Platelet activating factor (PAF): A review of its effects, antagonists and ossible future clinical implications (Part I). Drugs 1992;42(1):9-29 Koltain M et al. Platelet activating factor (PAF): A review of its effects, antagonists and possible future clinical implications (Part II). Drugs 1991 42(2):174-204 Schmidt U, Rabinovici K, Lande S. Einfluss eines ginkgo biloba specialekstraktes auf doe befomdlickeitbeizerebraler onsufficiziens. Muench Med Wochenschr 1991;133(suppl I):S15-18 Bruchert E, Heinrich SE, Ruf-Kohler P. WirksamkeitvonL11370bei. Alterenpatienten mit himleistungsschwache: multizentrishe doppelblindstudie des fachverbandes deutscher allegemeinaezte. Muench Med Wochenschr 1991;133(Suppl 1):S9-114 Meyer B. Etude multicentrique randomisee a double insu face au placebo due traitment des acouphenes per lextrait de ginkgo biloba. Presse Med 1986;15:1562-4 Taillandier J et al. Traitment des troubles du vidillissement cerebral pal Lextrait ginkgo biloba. Presse Med 1986;15:1583-7 Haguenauer JP et al. Traitment des troubles de lequilibre par lextrait ginkgo biloba. Presse Med 1986;p1569-72 Vorberg G, Schmidt U, Schenk N. Wirsamkeit eines neuen ginkgo biloba ekstraktes bei 100 patienten mi zerabraler insuffiziens. Herg Geffasse 1989;9:936-41 Eckmann F, Himleistungsstorungen Behandlung mit ginkgo biloba extract. Forsch Med 1990;108:557-60 Wesnes K et al. A double-blind placebo-controlled trial of tanakan in the treatment of idiopathic cognitive impairment in the elderly. Hum Psychopharmacol 1987;2:159-69
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19. Gessner B, Voelp A, Klasser M. Study of the long-term action of a ginkgo biloba extract on vigilance and mental performance as determined by means of quantitative measurements. Arzneimittel Forsch 1985;35:1459-65 20. Hofferberth B. Effect of ginkgo biloba extract on neurophysiological and psychometric measurement sin patients with cerebroorganic syndrome A double-blind study versus placebo. Arzneimittel-Forsch 1989;39:918-22 21. Hindmarch I, Subhan Z. The psychopharmacological effects of ginkgo biloba extract in normal healthy volunteers. Int J Clin Pharmacol Res 1984;4:89-93 22. Lanthony P, Cosson JP. Evolution de la vision des couleurs dand la retinopathie diabetique debutante traitee par extrait de ginkgo bilova. J Fr Ophtalmol 1988;11:671-4 23. Schneider B. Ginkgo biloba extract in peripheral arterial diseases: Meta-analysis of controlled clinical studies. Arzneimittel-Forsch 1992;42:428-36 24. Thomson GL et al. A clinical trial of ginkgo biloba extract in patients with intermittent claudication. Int Angiol 1990;9:75-8 25. Saudreau F et al. Efficacy of ginkgo biloba extract in the treatment of lower limb obliterative artery disease at stage III of the fontaine classification. J Mal Vasc 1989;14:177-82 26. Rudofsky VG. The effect of ginkgo biloba extract in cases of arterial occlusive disease: A randomized placebo controlled doubleblind crossover study. Forsch Med 1987;105:397-400 27. Bauer U. Ginkgo biloba extract in the treatment of arteriopathy of the lower limbs: Sixty-five week study. Presse Med 1986;15:1546-9 28. Bauer U. Six-month double-blind randomized clinical trial of ginkgo biloba extract versus placebo in two parallel groups in patients suffering from peripheral arterial insufficiency. Arzneimittel Forsch 1984;34:716-21 29. Murray MT. The Healing Power of Herbs (2nd ed.) Prima Publishing 1995 30. LeBars PL et al. A placebo-controlled double-blind randomized trial of an extract of ginkgo biloba for dementia. North American EGB Study Group. JAMA 1997;278(16):1327-32 31. Oken BS et al. The efficacy of ginkgo biloba on cognitive function in Alzheimer disease. Arch Neurology 1998;55(11):1409-15 32. Braquet P. Anti-anaphylactic properties of BN 52021: A potent platelet activating factor antagonist. Advances in Experimental Medicine and Biology 1987;215:215-33 33. Braquet P et al. Ethnopharmacology and the development of natural PAF antagonists as therapeutic agents. J Ethnopharmacol. April 1991;32(1-3):135-9 34. Rosenblatt M, Mindel J. Spontaneous hyphema associated with ingestion of ginkgo biloba extract. N Engl J Med. April 10 1997;336(15):p1108 35. Rowin J, Lewis SL. Spontaneous bilateral subdural hematomas associated with chronic Ginkgo biloba ingestion. Neurology. June 1996;46(6):1775-6 36. Kleijnen J et al. Ginkgo biloba. Lancet 1992;340(8828):1136-9 37. White HL et al. Extracts of ginkgo biloba leaves inhibit monoamine oxidase. Life Sci 1996;58(16):1315-21 38. Natural Product Encyclopedia. www.consumerslab.com:Ginkgo Biloba
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Ginseng
General Features
Asian Ginseng is a member of the Araliaceae family, which also includes the closely related American Ginseng and less similar Siberian Ginseng. The root of the plant is used for medicinal purposes, preferably from plants older than six years of age. There are three distinct types of Ginseng in the commercial market: 1. Panax Ginseng (Asian, Chinese, Korean Ginseng) 2. Siberian Ginseng (Eleuthero Ginseng) 3. American Ginseng (Panax quinquefolius, Canadian Ginseng) Panax Ginseng is the most widely used and most extensively studied species of Ginseng. Primarily the roots of the plant are used for medicinal purposes with standardized extracts available containing up to 5 percent ginsenoside content, in a high quality root extract product. Ginsenosides, which are triterpenoid saponins, vary between Panax, and American Ginseng. There are at least 13 different ginsenosides, some occurring more in one type of Ginseng than the other, or not at all as is sometimes the case. At this time, insufficient research exists to determine which type of Ginseng or ginsenoside complex is best suited to treat or prevent specific health conditions. However, studies reveal that the most consistent and reliable results occur when using high-quality extracts, standardized for active constituents. Siberian Ginseng contains seven eleutherosides (A-G), not ginsenosides.
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In Russia, Siberian Ginseng is used by deep sea divers, mine and mountain rescue workers, soldiers, factory workers, cosmonauts, and athletes primarily for its perceived ability to increase endurance and promote the bodys ability to tolerate stressful conditions.9 Studies with Panax Ginseng suggest that anti-fatigue effects may be mediated by stimulation of nerve impulses, direct affect on the hypothalamus-pituitary-adrenal axis, glycogen sparing in exercising muscle, and improved oxygen utilization. In animal studies, lower lactic acid and pyruvic acid levels in the blood were noted upon exercise, compared to the placebo group indicating a glycogen sparing effect through increased fatty acid oxidation during exercise.1, 2 These effects may be beneficial for endurance athletes and weight loss patients employing an exercise program. 10, 11, 12 A few studies have noted a performance-enhancing effect with the use of Panax Ginseng.12 2. Immunostimulating Effects In general, all three types of Ginseng demonstrate an ability to enhance immune system function. In particular Panax Ginseng appears to enhance antibody response, increase natural killer cell activity, stimulate macrophage activity, stimulate lymphocytes in vitro, stimulate the reticuloendothelial system, increase proliferation of T cells and B cells, and increase the production of interferon. 1, 2, 13, 14, Both Panax Ginseng and Siberian Ginseng have demonstrated enhanced immune function in placebo-controlled, double blind studies, including significantly higher antibody litres and natural killer activity levels in the Panax Ginseng study.15, 20 However, it should be noted that at high doses there is in vitro evidence that Ginseng may inhibit some immune functions, including lymphocyte proliferation.16, 17, 18, 19 Based upon the available research in this area, some authorities suggest that Ginseng supplementation is appropriate for chronic fatigue syndrome, HIV-infection, to combat infections or to help restore immune function from a compromised state.1, 2, 21 3. Female Reproductive Tissue Support Ginsenosides exert an estrogen-like action on the vaginal epithelium, which can prevent atrophic vaginal changes associated with menopause.22 It should be noted that breast tenderness can be a side effect of Ginseng use in women, which disappears when Ginseng is discontinued.23 N.B.: Black cohosh also maintains the vaginal epithelium without risk of this side effect (see Black Cohosh in this document) 4. Male Reproductive Tissue Support Panax Ginseng has been shown to increase sperm count and motility in men, as well as increasing plasma total and free testosterone, dihydrotestosterone, follicle stimulating hormone and leutinizing hormone. 24 An in vitro study suggests that it may relax the corpus cavernosum by releasing nitric oxide, which facilitates an erection. 25, 31 5. Type II Diabetes Panax and American Ginseng have demonstrated an ability to reduce fasting and post prandial blood glucose levels in type II diabetic patients. Its effects may alter the need or the dose of hypoglycemic medications and therefore, should only be used in this instance with knowledge of the attending physician.26, 27 6. Protection from Radiation Damage In experimental studies Ginseng has been shown to offer some protection against harmful radiation. 2 In particular, Siberian Ginseng is noted for its ability to provide protection in animals subjected to both single exposure and longterm x-ray radiation. Rats given the Siberian Ginseng have been shown to survive twice or three times as long compared to rats not given Siberian Ginseng, in radiation studies.28, 29
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Although no human trials in North America are available, Siberian Ginseng is thought to be useful as an adjunctive treatment for those undergoing radiation treatment for a variety of cancerous conditions. 1 Preliminary studies in Russia indicate that the use of Siberian Ginseng in people undergoing chemotherapy and radiation therapy for cancer has been of benefit in reducing side effects and aiding in bone marrow recovery. 30 N.B.: Note that Reishi Mushroom Extract and Astragalus are also known to reduce side effects from radiation treatment (see details in related sections of this document)
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Emphysema Cardiac disorders Patients suffering from mania, schizophrenia Insulin dependent diabetes mellitus Fibrocystic Breast Desease1,2,33 Caution must be exercised when administering Ginseng supplements: to type II diabetics as an adjunct to chemotherapy or radiation therapy1, 2, 33 at the same time as caffeine-containing beverages due to potential over stimulation effects. 21, 38
Drug-Nutrient Interactions
Ginseng is contraindicated in patients on the following medications: 1. Drugs affecting brain neurotransmitters, especially monoamine oxidase inhibitors (MAO-inhibitors): Ginseng can potentiate the drug effect leading to headache, euphoria, Central Nervous System stimulation and tremors, mania symptoms.34 2. Phenobarbital 5 3. Warfarin Ginseng has been shown to antagonize the clotting effects of warfarin, altering the prothrombin time or INR.35, 36 4. Ticlopidine a platelet-inhibiting drug. Similar effects on clotting due to Ginseng intake may counter effect of this drug, used by patients with intermittent claudication or to prevent stroke.21 5. Digoxin or Digitalis Ginseng has been shown to elevate serum levels of digoxin, potentiating the drugs effect on the heart.35, 37 This occurred in one case and no clear relationship exists, but caution should be exercised. 37 N.B.: Several studies performed in various countries have repeatedly shown that a high percentage of commercially available Ginseng supplement products do not meet the label claim for the amount of Ginseng, ginsenosides or active constituents they claim to possess. Furthermore, several cases of athletes consuming adulterated Ginseng products (i.e. ephedrine, pseudoephedrine) have occurred in which athletes have incurred doping charges against them and disqualification.39, 40, 41, 42, 43 As such, it is recommended that Ginseng products used for the intended purposes mentioned here, have available to health practitioners and consumers, certificate of analysis on each new batch of product formulated, to ensure potency and purity of the product.39-43 High quality Ginseng raw materials are expensive and thus may encourage some manufacturers to use inferior grades or to adulterate their products with cheaper ingredients (e.g., ephedra, caffeine) to simulate the anti-fatigue, performance-enhancing effects of Ginseng. Use with caution with patients on anti-asthmatic and antihypertensive drugs, as Ginseng may potentiate the effects of these drugs. As such, appropriate patient monitoring under these conditions is recommended.11,19
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19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37.
Boon H, Smith M. The Botanical Pharmacy. Quarry Health Books 2000:180-99 Murray M. The healing Power of Herbs. Prima Publishing 1995:265-79, 314-20 Chang H, But P. Pharmacology and Applications of Chinese Materia Medica. World Scientific, Philadelphia PA 1986:p773 Teegarden R. Chinese Tonic Herbs. Japan Publishing Inc NY 1985:p197 Bensky D, Gamble A. Chinese Herbal Medicine Materia Medica. Eastland Press, Seattle WA 1986:p556 Fulder SJ. Ginseng and the hypothalmic-pituitary control of stress. American Journal of Chinese Medicine 1981;0:112-8 Hiai S, Yokoyama H Oura H. Features of ginseng saponins-induced corticosterone secretion. Endocrinologia Japonica 1979;26:737-40 Hiai S, Yokoyama H, Oura H, Kawashima Y. Evaluation of corticosterone secretion-inducing effects of ginsenosides and their prosapogenins and sopogenins. Chemical and Pharmaceutical Bulletin 1983;31:168-74 Fulder S. The drug the builds Russians. New Science 1980;21:576-9 Avakian EV et al. Effect of panax ginseng on energy substrates during exercise. Fed Proc 1980;39:287 Avakian EV et al. Effect of panax ginseng extract on erergy metabolism during exercise in rats. Planta Medica 1984;50:p151 McNaughton L et al. A comparison of Chinese and Russian ginseng as ergogenic aids to improve various factets of physical fitness. Int Clin Nutr Rev 1989;9:32-7 See DM, Broumand N, Sahl L, Tilles JG. In vitro effects of Echinacea and ginseng on natural killer and antibody-dependent cell cytotoxicity in healthy subjects and chronic fatigue syndrome or acquired immunodeficiency syndrome patients. Immunopharmacology 1997;35(3):229-35 Liu J, Wang S, Liu H et al. Stimulatory effect of saponins from Panax ginseng on immune function of lymphocytes in the elderly. Mechanisms of Ageing and Development 1995;83(1):43-53 Bohn B, Nebe CT, Birr C. Flow-cytometric studies with Eleutherococcus senticosus extract as an immunomodulatory agent. Arzneimittelforschung 1987;37(10):1193-6 Jie YH, Cammisuli S, Baggiolini M. Immunomodulatory effects of Panax ginseng C.A. Meyer in the mouse. Agents and Actions 1984;15:386-91 Yun TK, Yun YS, Han IW. Anti-carcinogenic effect of long-term oral administration of newborn mice exposed to various chemical carcinogens. Cancer Detection and Prevention 1983;6:515-25 Yeung HW, Cheung K, Leung KN et al. Immunopharmacology of Chinese medicine. I. Ginseng-induced immuno suppression in virus infected mice. American Journal of Chinese Medicine 1982;10:44-54 Kang M, Yoshimatsu H, Oohara A et al. Ginsenoside Rg1 modulates ingestive behavior and thermal response induced by interleukin-1 beta in rats. Physiology and Behaviour 1995;57(2):393-6
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38. Scaglione F, Cattaneo G, Alessandria M, Cogo R. Efficacy and safety of the standardized Ginseng extract G115 for potentiating vaccination against the influencza syndrome and protection against the common cold. [Published erratum appears in Drugs Exp Clin Res 1996;22(6):p338]. Drugs Under Experimental and Clinical Research 1996;22(2):65-72 39. Healthnotes Online. Healthnotes Inc. 2000; www.healthnotes.com: Ginseng 40. Punnonen R, Lukola A. Oestrogen-like effects of ginseng. British Mecial Journal 1980;281:p1110 41. Palmer BV, Montgomer ACV, Monteiro JC. Ginseng and mastalgia. [Letter] British Medical Journal 1978;1:p1284 42. Salvati G, Genovesi G, Marcellini L et al. Effects of Panax Ginseng: C.A. Meyer, Saponins on male fertility. Panminerva Med 1996;38(4):249-54 43. Chen, X, Lee TJ. Ginsenosides-induced nitric oxide-mediated relaxation of the rabbit corpus cavernosum. British Journal of Pharmacology 1995;115(1):15-8 44. Sotaniemi EA, Haapakoski E, Rautio A. Ginseng therapy in non-insulin-dependent diabetic patients. Diabetes Care 1995;18(10):1373-5 45. Vukson V et al. American ginseng reduces postprandial glycemia in nondiabetic subjects and subjects with type 2 diabetes mellitus. Arch Int Med 2000;160:1009-1013 46. Farnsworth NR, Kinghorn AD, Soejarto D, Waller DP. Siberian ginseng (Eleuthrococcus sentricosus): Current status as an adaptogen. In: Wagner H, hikino H, Farnsworth NR, eds. Economic and Meidicinal Plant Research. Academic Press Orlando FL: 1985:155-215 47. Ben-Hur et al. Effect of Panax ginseng and Eleutherococcus S. on survival of cultural mammalian cells after ionizing radiation. Am J Chin Med 1981;9:48-56 48. Kupin VI et al. Stimulation of the immunological reacitivty of cancer patients by eleutherococcus extract. Vopr Onkol 1986;32:21-6 [in Russia] 49. Salvati G et al. Effects of Panax ginseng C.A. Meryer saponins on male fertility. Panminerva Med 1996;38:249-54 50. Colgan M. Optimum Sports Nutrition. Advanced Research Press 1993:p310 51. Brown DJ. Herbal Prescriptions for Better health. Prima Publishing Rocklin CA 1996;129-38 52. Miller LG. Herbal Medicinals: Selected clinical considerations focusing on known or potential drug-herb interactions. Arch Intern Med 1998;158(20):2200-11
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Drug-Nutrient Interactions
1. Paclitaxel: The efficacy of this chemotherapy drug is diminished by the ingestion of Goldenseal and therefore, should not be taken concurrently with this medication. 11 2. Tetracycline and Doxycycline: Berberine has been shown to reduce the absorption of tetracycline and possibly other antibiotics in one study, and appears to diminish the antibiotic effect of tetracycline against cholera. Thus, it may not be wise to use Goldenseal concurrently with antibiotic therapy. 12
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1.
Leung AY, Encyclopedia of Common Natural Ingredients Used in Food, Drugs, and Cosmetics, John Wiley & Sons: New York, 5252, 1980, 189-190. 2. Boon H and Smith M, Health Care Professional Training Program in Complementary Medicine, Institute of Applied Complementary Medicine Inc, 1997, 204-207. 3. Kumazawa T, et.al., Activation of Peritoneal Macrophages by Berberine Alkoloids in Terms of Induction of Cytostatic Activity, Int J Immunopharmacol 6, 1984, 587-592. 4. Sabir M, et.al., Further Studies on Pharmacology of Berberine, Indian J Physiol Pharmacol 22, 1978, 9-23. 5. Murray M, The Healing Power of Herbs (2nd edition), Prima Publishing, 1995, 162-172. 6. Kumazawa Y, et.al., Activation of Peritoneal Macrophages by Berberine Alkaloids in Terms of Induction of Cytostatic Activity, Int J Immunopharmacol 6, 1984, 587-592. 7. Mills S, The Essential Book of Herbal Medicine (2nd edition), London: Penguin Publishing, 1991, 677. 8. Lau CW, Yao XQ, Chen ZY et al. Cardiovascular actions of berberine. Cardiovasc Drug Rev. 2001; 19 (3): 234-44. 9. Principles and Practice of Phytotherapy. Mills S and Bone K. Churchill Livingstone Publishers. 2000: 294-295. 10. Chan E. Displacement of bilirubin from albumin by berberine. Biol Neonate. 1993; 63 (4):201-208. 11. Lin HL et al. Berberine modulates expression of Mdr1 gene product and the response of digestive tract cancer cells to paclitaxel. Br J Cancer. 1999; 81 (3): 416-22. 12. Healthnotes, Inc. 2001. www.healthnotes.com: Goldenseal
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3. Keloids and Other Connective Tissue Abnormalities There are numerous clinical reports and preliminary studies that suggest that Gotu Kola Extract can be useful in the treatment of keloid scars, anal fissures, periodontal disease, scleroderma, cellulite, and liver cirrhosis. 24,25 Experimental evidence has shown that the saponin constituents of Gotu Kola are able to stimulate the maturation of the scar by production of type I collagen, with a resulting decrease in the inflammatory reaction and myofibrinoblast production. 26 The net result is a scar that is less thick, more fine in its appearnce, and more visually acceptable in the mind of patients. Some authorities promote the use of Gotu Kola as part of a scar and keloid management program.26 Overall, there is a growing body of evidence that suggest that Gotu Kola Extract is an appropriate intervention for cellulite, keloid prevention and management, and may be useful in the treatment of a variety of connective tissue disorders. 2,3,4,5,6,7,8,9,10,11,12,13,17 For the prevention of keloid scars, Gotu Kola Extract is usually taken for 3 months prior to surgery, and for another 3 months afterwards. 17 4. Topical Application in Wound Healing and Burn Management Animal studies demonstrate that a Gotu Kola Purified Extract, containing high concentrations of asiaticoside, can enhance wound healing. 17 One preliminary trial in human subjects showed that Gota Kola Extract helped the healing of infected wounds (unless they had reached the bone level). 27 A significant number of studies originating in France have also shown that the topical application of Gotu Kola Extract can help heal various types of wounds.
28
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Drug-Nutrient Interactions
There are no well-known drug-nutrient interactions for Gotu Kola.
15, 16
Bourguigon D, Study of the Action of Titrated Extract of Centella Asiatica, Gaz Med Fr 82, 1975, 4579-4583. Bonnett GF, Treatment of Localized Cellulitis with Asiaticoside Madecassol, Prog Med 102, 1974, 109-110. Grosshans E and Keller F, Cellulite: Reality or Imposter?, J Med Strasbourg 14, 1983, 563-567. Keller F and Grosshans E, Cellulities: Reality or Fraud? Med Hyg 41, 1983, 1513-1518. Tenailleau A, On 80 Cases of Cellulities Treated with the Standard Extract of Centella Asiatica, Quest Med 31, 1978, 919-924. Carraro Pereira I, Treatment of Cellulitis with Centella Asiatica, Folha Med 79, 1979, 401-404. Guarnerio F, et.al., Treatment of Hemorrhoids with Centella Asiatica, G Ital Angiol 6, 1986, 46-52. Benedicenti A, Galli D, and Merlini A, The Clinical Therapy of Periodontal Disease: The Use of Potassium Hydroxide and the WaterAlcohol Extract of Centella Asiatica in Combination with Laser Therapy in the Treatment of Severe Periodontal Disease, Parodontol Stomatol 24, 1985, 11-26. Castellani C, et.al., Asiaticoside and Cicatrization of Episiotomies, Bull Fed Soc Gynecol Obstet 18, 1966, 184-186. Collonna dIstria J, Research on the Healing Action of Madecassol in Cervical and Laryngeal Surgery After Ionizing Radiations, J Fr Otorhinolaryngol 19, 1970, 507-510. OKeeffe P, A Trial of Asiatiocoside on Skin Graft Donor Areas, Br J Plast Surg 27, 1974, 194-195. Pignataro O and Teatini GP, Clinical Research on the Cicatrizing Action of Madecassol in Comparison of Oropharyngeal Mucosa, Minerva Med 56, 1965, 2683-2686. Rui R, et.al., Clinical Study of Madecassol in Otorhinogoly, J Med Lyon 47, 1966, 693-706. Sevin P, Some Observations on the Use of Asiaticoside (Madecassol) in General Surgery, Prog Med (France) 90, 1962, 23-24. Murray MT, The Healing Power of Herbs (2nd edition), Prima Publishing. Healthnotes, Inc. 2001.www.healthnotes.com: Gotu Kola. Natural Products Encyclopedia. www.consumerslab.com: Gotu Kola Laerum OD, Iversen OH. Reticuloses and epidermal tumors in hairless mice after topical skin application sof cantharidin and asiaticoside. Cancer Res 1972;32:1463-9
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19. Belcaro GV, Grimaldi R, Guildi G. Imrovement of capillary permeability in patients with venous hypertension after treatment with TTFCA. Angiology 1990;41:533-40 20. Belcaro FV, Rulo A, Grimaldi R. Capillary filtration and ankle edema in patients with venous hypertension treated with TTFCA. Angiology 1990;41:12-8 21. Cesarone MR, Laurora G, De Sactis MT et al. The microcirculatory activity of Centella asiatica in venous insufficiency. A double-blind study [translated from Italian]. Minerva Cardioangiol 1994;42:299-304 22. Pointel JP, Boccalon H, Cloarec M et al. Titrated extract of Centella asiatica (TECA) in the treatment of venous insufficiency of the lower limbs. Angiology 1987;38:46-50 23. Cesarone MR, Laurora G, De Sanctis MT et al. Activity of Centella asiatica in venous insufficiency [in Italian: English abstract]. Minerva Cardioangiol 1992; 40:137-43 24. Kartnig T. Clinical applications of Centella asiatica (L.) Urb. Herbs Spices Med Plants 1988;3:145-73 25. Bosse JP, Papillon J, Frenette G et al. Clinical study of a new antikeloid agent. Ann Plat Surg 1979;3:13-21 26. Widegerow AD, Chait LA, Stals R, et al. New innovations in scar management. Aesthetic Plast Surgery. 2000;24 (3):277-34. 27. Morisset R, Cote NG, Panisset JC et al. Evaluation of the healing activity of hydrocotyle tincture in the treatment of wounds. Phytother Res 1987;1:117-21 28. Kartnig T. Clinical application sof Centella asiatica 9L) Urb. In Herbs, Spices and Medicinal Plants: Recent Advances in Botany, Horticulture and Pharmacology, vol.3 Craker LE, Simon JE (eds.) Oryx Press Phoenix, AZ 1986:145-73
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High Cholesterol and/or Triglycerides Gugulipid was granted approval in India for marketing as a lipid-lowering drug in June 1986. Studies show that it lowers total cholesterol, LDL cholesterol, while elevating HDLcholesterol levels. (Agarwal RC, 1986 and Nityanand S, 1989). It appears that guggulsterones increase the uptake of LDL cholesterol from the blood by the liver. Studies in humans demonstrate that guggulsterone can produce a cholesterol reduction of 14-27%, in 4-12 weeks, and a 22-30% drop in blood triglyceride levels, in patients with hypercholesterolemia and/or hypertriglyceridemia. A striking feature is its lack of toxicity. Unlike other cholesterol lowering drugs, the administration of Gugulipid has not revealed any significant side effects, liver damage or toxicity, in human or animal studies to date.2,3,4,5,6,7,8,9,11,12 At least three well-controlled double-blind trials have shown that the oral administration of 75 100 mg of guggulsterone per day can significantly lower cholesterol and triglycerides, and improve the LDL to HDL-cholesterol ratio, in a manner that is associated with a reduced risk of heart disease and related cardiovascular disorders. One of these trials tested Gugulipid against the cholesterol lowering drug clofibrate, in a study involving 228 hypercholesterolemic patients. Results showed that the standardized grade of Gugulipid was equal in its effects to clofibrate in its ability to lower cholesterol levels and improve the lipid profile. 6,8,15 Experimental evidence indicates that guggulsterone lowers cholesterol, in part, by enhancing the uptake of excess serum LDL-cholesterol particles by the liver. This is accomplished through receptor-mediated endocytosis, located on the surface of the liver cell membranes. Rat liver exhibits up to an 87% increase in binding sites for human 1251- LDL with exposure to guggulsterones. Studies such as these imply that guggulsterones increase the catabolism of LDL-cholesterol as a primary mechanism through which it acts to lower blood cholesterol levels. 9 Of note is the fact that experimental studies reveal that Gugulipid also reduces oxidation of LDL-cholesterol via its antioxidant properties which may further provide protection against cardiovascular disease, as oxidized LDLcholesterol (modified LDL-cholesterol) has been shown to get deposited in the artery wall (narrowing blood vessels) to a much greater extent than non-oxidized LDL-cholesterol lipoproteins. 16 Gum Guggul has also been shown to reduce the stickiness of blood platelets, which is another biological action associated with reduced risk of cardiovascular disease. 17
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2. Anti-inflammatory Effects In experimental animal models, Gum Guggul demonstrates one-fifth the anti-inflammatory potency as hydrocortisone and the equivalent anti-inflammatory potency as phyenylbutazone and ibuprofen.10 In Ayurevedic medicine Gum Guggul has been used for this purpose, but no well-controlled trials on humans are available to firmly establish its application in the treatment of arthritic and other inflammatory joint conditions. 11,13 3. Acne The lipid lowering effect of Gum Guggul may help to control cystic acne, according to one of its traditional applications by Ayruvedic practitioners. One small clinical trial reported in 1994, tested Gum Guggul against the antibiotic drug tetracycline for the treatment of cystic acne. The results showed that Gum Guggul compared favorably in its effects to outcomes realized by patients treated with tetracycline. 18
Drug-Nutrient Interactions
1. Hypolipidemic Drugs: Gum Guggul may potentiate the cholsesterol lowering and triglyceride-lowering effects of these medications, enabling the attending physician to lower the dose or eliminate the need for these drugs, and in doing so, reduce the likelihood of side effects from these medications. 19,20,21 2. Anticoagulant Drugs: Gum Guggul may potentiate the effects of these drugs, and thus, proper patient monitoring of prothrombin time (INR) should be adhered to if Gum Guggul is used concurrently with anticoagulants such as, aspirin, warfarin, coumadin, plavix etc. 22 3. Thyroid Medications: Some studies suggest that Gum Guggul may stimulate the thyroid gland, which in turn, may alter the dosing requirement of thyroid medications. 23,24 4. Gum Guggul may reduce the absorption of the following drugs if taken at the same time: 5. Propranol 25 6. Calcium Channel Blockers (e.g, Diltiazem) 26
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1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.
Murray MT, The Healing Power of Herbs (2nd edition), Prima Publishing, 1995. Satyavati GV, A Primising Hypolipidaemic Agent from Gum Guggul (Commiphora Wightii), Econ Med Plant Res 5, 1991, 47-82. Nityand S and Kapoor NK, Hypocholesterolemic Effect of Commiphora Mukul Resin, Indian J Exp Biol 9, 1971, 376-377. Kuppurajan K, et.al., Effect of Gugglu on Serum Lipids in Obese Hypercholesterolemic and Hyperlipidemic Cases, J Assoc Physicians India 26, 1978, 367-371. Malhotra SC, Ahuja MMS, and Sundaram KR, Long Term Clinical Studies on the Hypolipidaemic Effect of Commiphora Mukul (Guggulu) and Clofibrate, Indian J Med Res 65, 1977, 390-395. Verna SK and Bordia A, Effect of Commiphora Mukul (Gum Guggulu) in Patients of Hyperlipidemia with Special Reference to HDL cholesterol, Indian J Med Res 87, 1988, 356-360. Agarwal RC, et.al., Clinical Trial of Gugulipid a New Hypolipidemicagent of Plant Origin in Primary Hyperlipidemia, Indian J Med Res 84, 1986, 626-634. Nityanand S, Srivastava JS, and Asthana OP. Clinical Trials with Gugulipid, a New Hypolipidaemic Agent, J Assoc Physicians India 37, 1989, 321-328. Singh V, et.al., Stimulation of Low Density Lipoprotein Receptor Activity in Liver Membrane of Guggulsterone Treated Rats, Pharmocol Res 22, 1990, 37-44. Sharma JN and Sharma JN, Commparison of the Anti-inflammatory Activity of Commiphora Mukul (an indigenous drug) with those Pfhenylbutazone and Ibuprofen in Experimental Arthritis Induced by Mycobacterial Adjuvant, Arzneimittel-Forsch 27, 1977, 1455-1457. Dietary Supplement Information Bureau. www.content.intramedicine.com: Guggul. Natural Health Products Encyclopedia. www.consumerslab.com: Guggul. Healthnotes, Inc.200.www.healthnotes.com: Guggul Satyavati GV. Gum guggul (Commiphora mukul) The success of an ancient insight leading to a modern discovery. Indian J Med 1988;87:327-35 Singh RB, Niaz MA, Ghosh S. Hypolipidemic and antioxidant effects of Commiphora mukul as an adjunct to dietary therapy in patients with hypercholesterolemia. Cardiovasc Drugs Ther 1994;8:659-64 Singh K, Chander R, Kapoor NK. Guggulsterone, a potent hypolipidaemic, prevents oxidation of low density lipoprotein. Phytother Res 1997;11:291-4 Mester L, Mester M, Nityanand S. Inhibition of platelet aggregration by guggulu steroids. Planta Med 1979;37:367-9 Thappoa DM, Dogra J. Nodulocystic acne: oral gugulipid versus tetracycline. J Dermatol 1994;21:729-31 Satyavati GV et al. Experimental studies on the hypocholesterolemic effect of commiphora mukul. Indian J Med Res 1969;57(10):1950-62
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20. Nityanand S et al. Clinical trials with gugulipid. A new hypolipidaemic agent. J Assoc Physicians India 1989;37(5):323-8 21. **Satyavati GV et al. Guggulipid: a promising Hypolipidemic agent from gum guggul (Commiphora Wightii). Econ Med Plant Res 1991;5:48-82 22. **Satyavati GV et al. Guggulipid: a promising Hypolipidemic agent from gum guggul (Commiphora Wightii). Econ Med Plant Res 1991;5:48-82 23. Tripathi YB et al. Thyroid stimulatory action of (Z)-Guggulsterone: mechanism of action. Planta Med 1988;54(4):271-7 24. Panda S, Kar A. Gugulu (Commiphora mukul) induces triiodothyronine production: possible involvement of lipid peroxidation. Life Sci 1999;65(12):PL137-41 25. **Dalvi SS et al. Effects of gugulipid on bioavailability of diltiazem and propranolol. J Assoc Physicians India 1994;42(6):454-5 26. **Dalvi SS et al. Effects of gugulipid on bioavailability of diltiazem and propranolol. J Assoc Physicians India 1994:42(6):454-5
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High Blood Pressure: Inhibits Angiotensin Converting Enzyme (acting as an ACE-inhibitor) by inhibiting the angiotensin-converting enzyme Hawthorn extract reduces the conversion of angiotensin I to angiotensin II, which is a potent constrictor of blood vessels and stimulates adrenal production of aldosterone. Thus, in a similar fashion to ACE-inhibitor drugs, Hawthorn extract has been shown to exert a blood pressure lowering effect. However, Hawthorn has been shown to have a modest effect on lowering blood pressure in hypertensive patients relative to more powerful ACE-inhibitor medications. In one study, systolic blood pressure dropped from 205 to 148 mm Hg, but other studies have shown a more modest reduction in blood pressure (e.g., systolic decline from 160 150 mm Hg, diastolic decline from 89 84 mm Hg) with Hawthorn extract supplementation. 7,11,15 Clinical trials show that Hawthorn extract can be an effective adjunct to the lowering of high blood pressure, but its hypotensive effects often require two to four weeks to manifest themselves. Hawthorn does not further lower blood pressure in subjects who demonstrate normal blood pressure, but rather selectively appears to reduce blood pressure only in hypertensive individuals. 23 Thus, the cardiovascular conditions that may be responsive to Hawthorn include congestive heart, angina, and high blood pressure. In particular, Hawthorn has a long history of use in the treatment of congestive heart failure. Congestive Heart Failure Clinical Trials: At least 8 double-blind, placebo-controlled trials, involving a total of more than 400 participants, have shown that Hawthorn extract is an effective intervention for mild to moderate congestive heart failure. 17 One study, involving more than 200 patients, found that Hawthorn extract was helpful in more severe congestive heart failure cases. 18 Even in more severe cases of congestive heart failure patients receiving high dose Hawthorn extract reported improvement in subjective symptoms ( shortness of breath, fatigue, etc.) as well as objective improvement in exercise capacity. 18 A comparative study has indicated that Hawthorn extract is about as effective as low dose captopril, a drug commonly used to treat congestive heart failure. 19 Hawthorn appears to act in a similar manner as other cardiac glycoside drugs, such as digoxin and digitalis, which exert an inotropic effect on the myocardium; enhancing ATP production through bioenergetic pathways. Studies reveal that Hawthorn provides similar benefits as these drugs, and exhibits a much safer profile. Digoxin and related cardiac glycoside prescription drugs increase the strength of the heart pump, but also increase the likelihood of dangerous arrhythmias. This occurs because these drugs shorten the refractory period between heartbeats (the period in which the heart can not contract between beats), which increases the chances of premature beats arising from areas outside or inside the hearts natural pacemaker. In turn, this disturbs the necessary synchronized and rhythmic contraction pattern that the heart muscle must follow to perform its function properly. The result is the development of cardiac arrhythmia, which can be life threatening. It is well documented that digoxin and related drugs have a narrow index of safety for this reason. In contrast to this, Hawthorn extract is able to strengthen the heart muscle, and has been shown to lengthen the refractory period between heartbeats, which reduces the likelihood of developing cardiac arrhythmias. As well, Hawthorn exhibits much lower toxicity than digoxin and is reported to have an enormously large range of safety, in regards to daily dosage (a number of studies have used doses as high as 600 mg per day with no significant side effects reported). 20,21,22, 13, 15 The major precautionary note pertains to the fact that it is not known if Hawthorn can be used safely with other cardiac glycoside drugs or with other medications (usually ACE- inhibitors) that are now more commonly prescribed in the treatment of congestive heart failure. 13 Some authorities suggest that Hawthorns effects are synergistic to the biological actions of cardiac glycoside drugs and ACE-inhibitors, indicating that they can be used concurrently as long as the attending physician is able to monitor patient response and adjust the dosing of these drugs accordingly. 15 From an historical standpoint, Hawthorn has been used alone and in combination with other cardiac glycoside drugs in the management of congestive heart failure.11, 15
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Anti- Aging: (Authors Note) Hawthorn may be an important herb in the prevention of cardiovascular disease and agerelated cardiac decline leading to the development of congestive heart failure. Studies demonstrate that after the age of 35- 40 the heart muscle appears to make less ATP energy in a certain percentage of individuals. This has been shown to result from a marked reduction in Coenzyme Q10 synthesis, which is required to maximize the conversion of ADP to ATP. Theoretically, supplementation with both Coenzyme Q10 and Hawthorn extract may help to stave off age-related declines in ATP production, due to their known inotropic effects on heart muscle. Many practitioners involved in anti-aging medicine subscribe to this practice and recommend these supplements on a preventive basis to their patients over 40 50 years of age. (see also Coenzyme Q10 in this document).
Drug-Nutrient Interactions
Hawthorn may potentiate the action of the following drugs, and therefore, requires appropriate physician monitoring if taken concurrently with these medications. This is extremely important in the case of digitalis, digoxin and other cardiac glycoside drugs, as it is plausible that a drug nutrient interaction of this nature could lead to life threatening consequences. Interactions of concern include: 1. Digitalis, digoxin and other cardiac glycoside medications 24 2. Antiarrhythmic Medications 25 3. Anti-hypertensive Medications: As Hawthorn extract is known to lower high blood pressure to some degree, it may work synergistically with a variety of antihypertensive drugs, reducing the required dosage of the drug. 26, 27
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1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.
Petkov V, Plants with Hypotensive, Antiatheromatous and Coronarodilating Action, Am J Clin Med 7, 1979, 197-236. Wagner H, Bladt S, and Zgainski EM, Plant Drug Analysis, Springer-Verlag, New York, 1984, 166 & 178-179. Ammon HPT, Handel M, Crataegus, Toxicology and Pharmacology, I Toxicity, Planta Medica 43, 1981, 105-120, II Pharmacodynamics, Planta Medica 43, 1981, 209-239, III Pharmacodynamics and Pharmacokinetics, Planta Medica 43(4), 1981, 313-322. Mavers VWH, and Hensel H, Changes in Local Myocardial Blood Flow Following Oral Administration of a Crataegus Extract to Nonanesthetized Dogs, Arzneimittel-Forsch 24, 1974, 783-785. Roddewig VC, and Hensel H, Reaction of Local Myocardial Blood Flow in Non-anaesthetic Dogs and Anesthetized Cats to Oral and Parental Application of Crataegus Fraction (Ologomer Procyanidins), Arzneimittel-Forsch 27, 1977, 1407-1410. Rewerski VW, et.al., Some Pharmacological Properties of Oligometric Procyanidin Isolated from Hawthorn (Crataegus Oxyacantha), Arzneimittel-Forsch 17, 1967, 490-491. Uchida S, et.al., Inhibitory Effects of Condensed Tannins on Angiotensin Converting Enzyme, Jpn J Pharmacol 43, 1987, 242-245. Blesken R, Crataegus in Cardiology, Forschr Med 110, 1992, 290-292. OConnoly VM, et.al., Treatment of Cardiac Performance (NYHA Stages I to II) in Advanced Age with Standardized Crataegus Special Extract, Forschr Med 104, 1986, 805-808. Leuchrgens H, Crataegus Special Extract WS 1442 in NYHA II heart failure. A Placebo Controlled Randomized Double-blind Study, Forschr Med 111, 1993, 352-354. Murray MT, The Healing Power of Herbs (2nd edition), Prima Publishing, 1995. Dietary Supplement Information Bureau.www. content.intramedicine.com: Hawthorn Natural Products Encyclopedia. www.consumereslab.com: Hawthorn Healthnotes, Inc. 2001. www.healthnotes.com: Hawthorn Principles and Practice of Phytotherapy. Mills M and Bone K. Churchill Livingstone.2000: 444-445 Wagner H et al. Cardioactive Drugs IV. Cardiotonic amines from crataegus oxyacantha. Planta Medica 1982;45:99-101 Weihmayr T, Ernst E. Therapeutic effectiveness of crataegus. Forschr Med 1996;114:27-9 Tauchert M. Efficacy and safety of crataegus extract WS 1442 in comparison with placebo in patients with chronic stable New York heart Association class-III heart failure. Am Heart J 2002;143(5):910-5 Tauchert M, Siegel G, Schulz V. Hawthorn extract as plant medication for the heart; a new evaluation of it therapeutic effectivenss [translated from German]. MMW Munch Med Wochenschr. 1994;136(suppl 1):S3-S5 Popping S, Rose H, Ionescu I et al. Effect of a hawthorn extract on contraction and energy turnover of isolated rat cardiomyocytes. Arzneimittelforschung 1995;45:1157-61
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21. Joseph G, Zhao Y, Klaus W. Pharmacolgic action profile of crataegus extract in comparison to epinephrine, amirinone, milrinone and digoxin in the isolated perfused guinea pig heart [in German; English abstract]. Arzneimittelforschung 1995;45:1261-5 22. Schulz V, Hansel R, Tyler VE. Rational Phytotherapy: A Physicians Guide to Herbal medicine. 3 rd ed. Berlin, Germany, Springer-Verlag 1998:91-4 23. Murray M, Pizzonro J. Encylopedia of Natural Medicine (2nd ed) Prima Publishing 1997:524-35 24. Petkov V. Plants and hypotensive, Antiatheromatous and coronarodilatating action. Am J Chinese Med 1979;7:197-236 25. Wagner H et al. Cardioactive Drugs IV. Cadiotonic amines from crataegus oxyacantha. Planta Medica 1982;45:99-101 26. Uchida S et al. Inhibitory effects of condensed tannins on agiotensin converting enzyme. Jap J Pharmacol 1987;43(2):242-6 27. Taskov M. On the coronary and cardiotonic action of crataemon. Acta Physiol Pharmacol Bulg 1977;3(4):53-7
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2. Prevention of Deep Vein Thrombosis Following Surgery Over a 3-year period, a controlled trial of 4,176 patients with thrombosis, lung infarction or lung embolism investigated prophylactic treatment for deep vein thrombosis and embolism arising from surgery. Patients received an intravenous injection of Horsechestnut extract (10 ml per day), strophantin or digitalis, Vitamin B complex and Vitamin C or a similar injection without Horsechestnut extract for 4 days prior to surgery and continuing for up to 7 days after the operation. Horsechestnut significantly reduced the incidence of deep vein thrombosis following surgery compared to the control group and other patients.1 3. Other Potential Applications These may include cerebral edema following cranial fractures and trauma, haemorrhoids, varicose veins (early stages), carpal tunnel syndrome 1,6 and possibly as a supplement to help prevent hemorrhage in diabetic retinopathy, and to support the small blood vessels in the macula of the eye in certain eye conditions. 4. Topical Application A topical gel containing 1.4-2% escin (triterpene glycoside) content has been used successfully to help treat chronic venous insufficiency, hematoma, contusions, non-penetrating wounds and sports injuries involving edema.1,4
Drug-Nutrient Interactions
Anticoagulant Medications (Warfarin, Coumadin Aspirin, etc.) - Experimental evidence suggests that Horsechestnut seed extract may potentiate the effects of anticoagulant drugs. However, there are no reports of bleeding disorders in humans to date, in subjects using Horsechestnut seed extract with or without concurrent anticoagulant therapy.
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Practitioners and patients should be mindful of this potential interaction, but it is not considered to be a contraindication to the use of Horsechestnut seed extract at this time.22,23,24
Mills S, Bone K. Principles and Practice of phytotherapy. Churchill Livingstone 2000;Horsechestnutseed:448-55 Schulz V et al. Rational Phytotherapy. Berlin:Springer-Verlag;1998:129-38 Chandler RF. Horse chestnut. Canadian Pharm J 1993;Jul/Aug:297-300 Dinsdale, M. Horse Chestnut. Better Nutriiton, Feb2000;62(2):32 Guillaume M, Padioleau F. Venotonic effect, vascular protection, anti-inflammatory and free radical scavenging properties of horse chestnut extract. Arzneim-Forsch Drug Res 1994;44:25-35 Sirtori, CR. Aescin: pharmacology, pharmacokinetics and therapeutic profile. Pharmacol Res 2001 Sep;44(3):183-93 Herbal Help for Tired Swollen Legs. Environmental Nutrition, Jun2001;24(6):p7 Brunner F, Hoffmann C, Schuller-Petrovic S. Responsivemenss of human varicose saphenous veins to vasoactive agents. Br J Clin Pharmacol 2001 Mar;51(3):219-24 Bone, Kerry. Phytotherapy Review & Commentary: Horse-chestnutA safe and effective vein treatment. Townsend Letter for Doctors & Patients, May2000;202:p152 Pittler, MH, Ernst E. Horse chestnut seed extract for chronic venous insufficiency. Cochrane Database Syst Rev 2002;(1):pp.CD003230 Pittler MH, Ernst E. Horse-chestnut seed extract for chronic venous insufficiency. A criteria-based systematic review. Arch Dermatol 1998 Nov;134(11):1356-60 Morien, K. Horse Chestnut Effective in Chronic Venous Insufficiency. HerbalGram, Winter 99;45:p22 Koch R. Comparative study of Venostasin and Pycnogenol in chronic venous insufficiency. Phytotherapy Res 2002 Mar;12(Suppl 1):S1-5 Rothkopf M, et al. New findings on the efficacy and mode of action of the horse chestnut saponins escin. Arzneim-Forsch/Drug Res 1976;26(2):225-35 **Guillaume M et al. Veinotonic effect, vascular protection, anti-inflammatory and free radical scavenging properties of horse chestnut extract. Arzneim-Forsch/Drug Res 1994;44(1):25-35 Tyler, VE. Herbs of Choice: The Terapeutic Use of Phytomedicinals. Binghampton, NY; Pharmaceutical Products Press, 1994:112-3
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17. Blumental M, Busse WR, Goldberg A et al. (eds.) The Complete Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, MA: Integrative Medicine Communications, 1988:148-9 18. Hellberg K, Ruschewski W, de Vivie R. Medikamentoes bedingtes post-operatives Nierenversagen nach herzchirugischen. Eingriffen. Thoraxchirurgie 1975;23:396-9 19. Wilhelm K, Feldmeier C. Postoperative und posttraumatische Oedemprophylaxe und-therapie. Laborchemische Untersuchungen ueber die Nierenvertraeglichkeit von beta-Aescin. Med Klin 1975;70:2079-83 20. Newall CA, et al. Herbal Medicines: A Guide for Health Care Professionals. London: The Pharmaceutical Press 1996:166-7 21. Heck AM et al. Potential interactions between alternative therapies and warfarin. Am J health Syst Pharm, Jul2000;57(13):1221-7 22. Heck AM, DeWitt BA, Lukes AL. Am J Helath Syst Pharm 2000 Jul 1;57(13):p1221-7;Quiz p1228-30 23. Akopov SE et al. Mechanisms of platelet-induced angioplastic reactions: Potentiation of calcium sensitivity. Can J Physiol Pharmacol. Jul 1997;75(7):849-52 24. Dworschak E et al. Medical activities of aesculus hippocastaneum (Horse-chestnut) Saponins. Adv Exp Med Biol 1996;404:471-4
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Huperzine A
General Features
Huperzine A is an extract from a club moss (from the Lycopodiaceae family) that has been used for centuries in Chinese folk medicine for a variety of conditions. In modern times Huperzine A research has focused on its ability to raise brain levels of the memory chemical acetylcholine, hence its potential role in the treatment and prevention of Alzheimers Disease, dementia and other cases of memory and learning impairment. 1, 2
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Biological Action HupA is rapidly absorbed by the brain where it acts as a potent, reversible and selective inhibitor of the enzyme acetylcholinesterase, which breaks down the memory chemical acetylcholine. By inhibiting this enzyme, brain concentrations of acetylcholine are increased, thereby facilitating improvements in memory and learning capacity. A hallmark feature of Alzheimers disease is reduced concentrations of acetylcholine in specific areas of the brain involved with memory and other cognitive functions. Huperzine A supplementation appears to help increase acetylcholine levels in Alzheimers patients in cases where the condition has not yet advanced to the point where brain cells are permanently damaged. Studies show that Huperzine A provides a longer acting effect than the drugs tacrine and doneprizil, which are used in Alzheimers disease, and it also appears to produce fewer side effects. This is due to the fact that only very small doses of Huperzine A are required due to its high specificity for the acetylcholinesterase enzyme. As such, HupA is under intensive investigation as a viable intervention in the prevention and treatment of Alzheimers disease, dementia, and other conditions involving learning and memory impairment.1,4,5,6 Further, it has recently been reported that HupA also reduces neuronal death (death of nerve cells) caused by glutamate (glutamate toxicity results in seizures associated with exposure to nerve gas), suggesting that HupA may act to protect brain cells from various types of degenerative damage and chemical insults. The dual bio-activities (preserving acetylcholine and protecting nerve cells) make HupA an attractive agent to study as a potentially important therapeutic agent for Alzheimers disease.1
Drug-Nutrient Interactions
Acetylcholinesterase Inhibitors, such as Donepezil and Tacrine - These drugs also inhibit the breakdown of acetylcholine and therefore, the addition of Huperzine A may potentiate their effects, increasing the likelihood of developing cholinergic syndrome as a serious side effect. 17,18 These drugs on their own are noted for the side effects of vomiting, excess saliva and tear production, and increased sweating, which indicate their tendency to over stimulate the cholinergic system.15
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Bai DL, et al. Huperzine A, a potential therapeutic agent for treatment of Alzheimers disease. Curr Med Chem, Mar2000;7(3):355-74 Dworkin N. Restoring memory. Psychology Today, Jul/Aug00;32(4):p28 Pirisi, Angela. Plant wisdom: Memory moss. Yoga Journal, 08/31/1999;147:p95 McCaleb R. Huperzia looks promising for improving memory. HerbalGram, 10/31/1995;35:p14 Tang XC. Huperzine A (shuangyiping): A promising drug for Alzheimers disease. Chung Kuo Yao Li Hsueh Pao, Nov1996;17(6):481-4 Ashani Y, Peggins JO, Doctor BP. Mechanism of inhibition of cholinesterases by huperzine A. Biochem Biophys Res Commun, 1992:184:719-26 Xu SS, Gao, ZX, Weng Z et al. Efficacy of tablet huperzine-A on memory, cognition, and behavior in Alzheimers disease. Chung Kuo Yao Li Hsueh Pao, 1995;16:391-5 Wang Z, Ren G, Zhao Y et al. A double-blind study of huperzine A and piracetam in patients with age-associated memory impairment and dementia. In: Kanba S, Richelson E (eds.) Herbal Medicines for Nonpsychiatric Diseases. Tokyo: Seiwa Choten Publishers, 1999:39-50 Cheng DH, Tang XC. Comparative studies of huperzine A, E2020, and tacrine on behavior and cholinesterase activites. Pharmacol Biochem Behav, 1998;60:377-86 Cheng DH, Ren H, Tang XC. Huperzine A, a novel promising acetylcholinesterase inhibitor. Neuroreport, 1996;8:97-101 Sun QQ, Xu SS, Pan JL, et al. Huperzine-A capsules enhance memory and learning performance in 34 pairs of matched adolescent students. Acta Pharmacol Sin, 1999;20:601-3 Qian BC, Wang M, Zhou ZF, et al. Pharmacokinetics of tablet huperzine A in six volunteers. Chung Kuo Yao Li Hsueh Pao, 1005;16:396-8 Huperzine A for memory enhancement? NCRHI Newsletter, 04/30/2000;23(2):3-4 [Pharmacists Letter] Current Medical Diagnosis and Treatment. 33rd Annual Revision, 1994. Lange Medical Books. Appleton and Lange:p1323 2001 Healthnotes, Inc. www.healthnotes.com: Huperzine A Skolnick AA. Old Chinese herbal medicine used for fever yields possible new Alzheimer disease therapy. JAMA, Mar1997;277(10):p776 Cheng DH et al. Huperzine A, a novel promising acetylcholinesterase inhibitor. Neuroreport, Dec1996;8(1):97-101 Liu J, et al. Inhibitory effects of huperzine B on cholinesterase activity in mice. Chung Kuo yao Li Hsueh Pao, Feb1999;20(2):141-4
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Of special note is the fact that unlike benzodiazepines, Kava does not seem to impair reaction time or alertness when taken in divided doses throughout the day for the treatment of anxiety, at recommended intake levels. 2. Insomnia Kava is known to have sedative effects at specific levels of intake, which have prompted its use as a natural treatment for insomnia. This effect is also considered to be mediated through its influence of the limbic system. 10 In one placebo-controlled study of 12 healthy volunteers Kava extract was shown to improve the ability to fall asleep at a dose of 300 mg per day (yielding 210 mg of Kava-lactone content). It also lengthened the deep sleep phase and shortened the wakeful phases in sleep, according to EEG recordings (electro-encephalogram). These effects are looked upon favorably compared to effects on sleep induced by benzodiazepines and barbituate drugs. Kava administration also increased the density of sleep spindles, an effect, which is comparable to medical sedative drugs. 26
Other investigations have implicated Kava as an agent that can produce liver injury. A survey of the aboriginal community in Australia revealed that heavy Kava users were at higher risk of developing liver damage, as evidenced by laboratory studies, than were non- users and occasional users of Kava. Risk of liver injury was directly related to the amount of Kava consumed. 35 In Germany, Canada and the United States, governments are have considered banning the use of Kava, due to reports from Europe indicating that taking Kava at recommended intake levels can induce severe liver injury, even
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in occasional users. At this time, Kava is still available without a prescription in many parts of the world, but experts suggest that individuals seek appropriate monitoring of liver enzymes by their physician if they intend to use this herbal agent on any level of frequency. Anyone with pre-existing liver disease or taking other drugs known to cause liver damage, or consuming alcohol on a regular basis, should avoid the use of Kava altogether. 11 On December, 18, 2001 the Food and Drug Administration (FDA) in the United States informed health care practitioners that it was launching an investigation to determine if Kava supplementation poses a health threat to human health. The agency noted that German and Swiss health authorities had reported approximately 25 cases of serious liver toxicity, related to Kava consumption. This initial communication was to serve as a data-gathering tool and was not issued as a warning or alert. Although there are currently no published reports of liver toxicity in the U.S., the FDA has indicated that it has received adverse event reports through its MEDWATCH system that potentially links Kava to liver damage. 41 Other Side Effects: Long-term use (few months to a year) can produce Kava dermopathy (scali skin eruptions) on the palms, soles, forearms, back and shins. High doses (7310 gms per week) may decrease serum albumin, protein, urea, bilirubin, platelet count and lymphocyte count.1,2,3,4 Kava may temporarily turn skin yellow, create mild gastrointestinal disturbances, induce an allergic skin reaction, such as a rash and/or produce pupil enlargement in long-term users. 28,36,37 Short-term Kava studies (4 7 weeks) at usual intake doses have not shown any significant side effects other than the occasional report of gastrointestinal upset or skin rash. 38 Acute Dystonic Reactions: Kava should not be use by individuals who have had acute dystonic reactions, which consist of spasms in the muscles of the neck and movements of the eyes. These problems are related to the neurotransmitter dopamine, according to popular beliefs, and are typically caused by antipsychotic drugs, which affect dopamine. Kava may trigger these reactions in patients with a known history of dystonic reactions. 40
Drug-Nutrient Interactions
Kava supplementation is reported to potentiate the effects of the following medications leading to excess sedation and thus, should not be taken concurrently: Sedative medications ( benzodiazepines)42, 43 Alprazolam a reported case possibly lead to coma in a patient combining Kava with this drug. 44 Antidepressant drugs 42 Diphenydramine an over-the-counter drug that induces sedation
41,42
Alcohol some reports suggest that Kava can increase alcohols damaging effects to the heart, nervous system, liver, immune system, kidneys and other organs. It is advisable not to combine Kava intake with the consumption of alcohol.
48,49,50
Antipsychotic drugs Kava may increase risk of dystonic reactions if combined with these drugs. 11 Levodopa patients with Parkinsons disease taking levodopa should avoid Kava as Kavas effects on the dopamine system may reduce the effectiveness of levodopa. 11
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Singh Y, Kava: An Overview, J Ethnopharmacol 37, 1992, 13-45. Holm E, et.al., Studies on the Profile of the Neurophysiological Effects of D.L.-kavain: Cerebral Sites of Action and Sleep-WakefulnessRhythm in Animals, Arzneimittel-Forsch 41, 1991, 673-683. Lindenberg D and Pitule-Schodel H, D, L-kavain in Comparison with Oxazepam in Anxiety Disorders. A Double-blind Study of Clinical Effectiveness, Forschr Med 108, 1990, 49-50, 53-54. Kinzler E, Kromer J, and Lehmann E, Clinical Efficacy of a Kava Extract in Patients with Anxiety Syndrome: Double-blind Placebo Controlled Study Over 4 Weeks, Arzneimittel-Forsch 41, 1991, 584-588. Warnecke G, Neurovegetative Dystonia in the Female Climacteric. Studies on the Clinical Efficacy and Tolerance of Kava Extract WS 1490, Forschr Med 109, 1991, 120-122. Norton SA and Ruze P, Kava Dermopathy, J Am Acac Dermatol 31, 1994, 89-97. Ruze P, Kava-induced Dermopathy: A Niacin Deficiency, Lancet 336, 1990, 1442-1445. Mathews JD, et.al., Effects of the Heavy Usage of Kava on Physical Health: Summary of a Pilot Survey in an Aboricinal Community, Med J Aust 148, 1988, 548-555. Healthnotes, Inc. 2001. www.healthnotes.com: Kava Dietary Supplement Information Bureau. www.content.intramedicine.com: Kava Natural Product Encyclopedia. www.consumerslab.com: Kava Meyer HJ, Kretzschmar R. Kawa pyronea new kind of substance group of central muscle relaxants of the mephenesin type [translated from German]. Klin Wochenschr 1966;44:902-3 Klohs MW, keller F, Williams RE et al. A chemical and pharmacological investigation of Piper methysticum Forst. J Med Pharm Chem 1959;1:95-103 Bruggemann VF, Meyer HJ. Studies on the analagesic efficacy of the kava constituents dihydrokavain (DHK) and dihydromethysticin (DHM) [in German; English abstract]. Arzneimittelforschung 1963;13:407-9 Jussofie A, Schmiz A, Hiemke C. Kavapyrone enriched extract from Piper methysticum as modulator of the GABA binding site in different regions of rat brain. Psychopharmacology (Berl) 1994;116:469-74 Boonen G, Haberlein H. Influence of genuine kavapyrone enantiomers on the GABAA binding site. Planta Med 1998;64:504-6 Volz HP, Kieser M. Kava-kava extract WS 1490 versus placebo in anxiety disordersa randomized placebo-controlled 25-week outpatient trial. Pharmacopsychiatry 1997;30:1-5 Kinsler E, Kromer J, Lehmann E. Effect of a special kava extract in patientw with anxiety-,tension-, and excitation states of non-psychotic genesis. Double blind study with placebos over 4 weeks [translated from German]. Arzneimittelforschung 1991;41:584-8
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19. Warnecke G, Pfaender H, Gerster G et al. Efficacy of an extract of kava root in patients with climacteric syndrome. A double blind study with a new mono-preparation [translated from German]. Z Phytother 1990;11:81-6 20. Warnecke G. Psychosomatic disorders in the female climacterium, clinical efficacy and tolerance of kava extract WS 1490 [translated from German]. Fortschr Med 1991;109:119-22 21. Malsch U, Klement S. Randomized placebo-controlled double-blind clinical trial of a special extract of kava roots (WS 1490) in patients with anxiety disorders of non-psychotic origin [abstract]. Eur Phytojournal [serial online]. 2000;1. Available at:http://www.escop.com/issue_1. Accessed May 10, 2001 22. Woelk H, Kapoula O, Lehri S et Al. The treatment of patients with anxiety. A double blind study: dava extract WS 1490 versus benzodiazepine [translated from German]. Z Allg Med 1993;69:271-7 23. Cropley M, Cave Z. Effect of kava and valerian on physiological responses to psychological stress assessed under laboratory conditions [abstract]. FACT 2001;6:76 24. De Leo V, la Marca A, Morgante G et al. Evaluation of combining kava extract with hormone replacement therapy in the treatment of postmenopausal anxiety. Maturitas 2001;39:185-8 25. Munte TF, Heinze HJ, Matzke M, Steitz J. Effects of oxazepam and an extract of kava roots (Piper methysticum) on event-related potentials in a word-recognicition task. Pharmacoelctroencephalog 1993;27:46-53 26. Principles and Practice of Phytotherapy. Mills S and Bone K. Churchill Livingstone. 2000: 456-58 27. Blumenthal M, Busse WR, Goldberg A et al. (eds.) The Complete Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston MA: Integrative Medicine Communications 1998:156-7 28. Jappe U, Franke I, Reinhold D, Golinick HPM. Sebotropic drug reaction resulting from kava-kava extract therapy: A new entity? J Amer Acad Dermatol 1998:38:104-6 29. Stafford, Ned. Germany may ban kava kava herbal supplement. Reuters Nov.19 2001 30. Escher M, Desmeules J, Giostra E, Mentha G. Hepatitis associated with kava, a herbal remedy for anxiety. BMJ 2001;322:p139 31. Kraft M, Spahn TW, Menzel J et al. [Fulminant liver failure after administration of the herbal antidepressant Kava-Kava.] Dtsch Med Wochenschr 2001;126:970-2 [in German]. 32. Strahl S, Ehret V, Dahm HH, Maier KP. [Necrotizing hepatitis after taking herbal remedies.] Dtsch Med Wochenschr 1998;123:1410-4 [in German] 33. Russmann S, Lauterburg BH, Helbling A. Kava hepatotoxicity. Ann Intern Med 2001;135:68-9 [letter] 34. Information provided by the German Federal Institute for Drugs and Medical Devices. 35. Mathews JD, Riley MD, Fejo L et al. Effects of the heavy usage of kava on physical health: summary of a pilot survey in an aboriginal community. Med J Aust 1988;148:548-55 36. Schmidt P, Boehncke WH. Delayed-type hypersensitivity reaction to kava-kava extract. Contact Derm 2000;42:363-4 37. Blumenthal M, Busse WR, Goldberg A et al (eds.) The Complete Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston MA: Integrative Medicine Communications 1998:156-7 38. Schulz V, Hansel R, Tyler VE. Rational Phytotherapy: A Physician Guide to Herbal Medicine. 3 rd ed. Berlin, Germany: SpringerVerlag;1998:p71 39. Schelosky L, Raffauf C, Jendroska K et al. Kava and dopamine antoginism [letter]. J Neurol Neurosurg Psychiatry 1995;58:639-40 40. National Nutritional Foods Association Update. December 21, 2001. Kava safety concerns raised. 41. Jussofie A et al. Kavapyrone enriched extract from piper methysticum as modulator of the GABA binding site in different regions of rat brain. Psychopharmacology (Berl). Dec 1994;116(4):469-74 42. Klohs MW. Chemistry of Kava. Psychopharmacol Bull 1967;4(3):p10 43. Almeida JC et al. Coma from the health food store: Interaction between Kava and Alprazolam. Ann Intern Med Dec1996;125(11):940-1 44. Jamieson DD et al. Positive interaction of ethanol and kava resin in mice. Clin Exp Pharmacol Physiol Jul1990;17(7):509-14 45. Cantor C. Kava and alcohol. Med J Aust Nov1997;167(10):p560 46. Herberg KW. Effect of Kava-special extract WS 1490 combined with ethyl alcohol on safety-relevant performance parameters. Blutalkohol Mar1993;30(2):96-105
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2. Anti-inflammatory Effects Licorice produces a cortisol like action, which inhibits the formation of certain inflammatory compounds. Glycyrrhetinic acid may also have a direct anti-inflammatory action by selectively inhibiting the classical complement cascade.1 To date, there have been no well-designed human trials demonstrating the efficacy of Licorice in the management of arthritis or other inflammatory conditions. Other herbal agents such as curcumin, white willow extract, boswellia, and ginger, have been used in clinical trials for these purposes with good success, and may therefore be more reliable interventions for these problems. (see details for each of these herbal agents in this document) 3. Liver Support and Protection Glycyrrhizin has been shown to be an effective treatment in the management of viral hepatitis. 1 In-vitro studies demonstrate that it protects the liver from damage caused by chemical toxins such as carbon tetrachloride, likely through the inhibition of the cytochrome P-450 enzyme system conversion of CCI4 to CCI3.1 The flavonoid content of Licorice has also been shown in experimental studies to protect liver cells from free radical damage through its antioxidant effects. 22 At present there are no well-designed human trials to demonstrate how useful Licorice might be in the management and treatment of liver conditions, whereas, natural agents such as N-acetylcysteine, Reishi Mushroom Extract, Milk Thistle, Dandelion and Trimethylglycine (Betaine) have been shown to be effective in clinical trials with patients suffering from various liver disorders. (see details for each of these natural agents in this document) 4. Peptic Ulcers In an attempt to reduce the side effects of Licorice, de-glycyrrhizinated Licorice (DGL) was developed. The flavonoid content of Licorice has been shown to exert a number of health-promoting effects to the alimentary tract by affecting parietal cell acid secretion, gastric mucosal prostaglandin production, and possibly the inhibition of Helicobacter pylori bacteria growth. For these reasons DGL has been tested as a treatment for peptic ulcers, and the available studies suggest it has healing properties for gastric (stomach) and duodenal ulcers. 26 Taken as a chewable tablet, Caved-S or Ulcedal have demonstrated remarkable success in treating gastric and duodenal ulcers. The results are comparable to the ulcer medications cimetidine and ranitidine commonly used in the treatment of gastric ulcers. Furthermore, these chewable Licorice tablets were shown to be equally, or more effective as these standard ulcer drugs in regards to preventing ulcer recurrence (one year follow-up). It appears that these tablets must mix with saliva in order to be effective, thus, swallowing Licorice capsules is ineffective in ulcer treatment.1,2 Chewing de-glycyrrhizinated Licorice chewable tablets may be seen as an effective complementary means of treating gastric and duodenal ulcers. DGL appears to stimulate the normal defense mechanisms that prevent ulcer formation. Specifically, DGL improves and enhances the quality and quantity of the protective coating that lines the intestinal tract, increases the life span of the intestinal cells, and improves blood supply to the intestinal lining. 13 Scientific evidence suggests that Licorice-derived compounds, other than glycchrizin, have the effect of raising the local concentration of those prostaglandins that promote mucus secretion and cell proliferation (through inhibition of 15- hydroxyprostaglandin dehydrogenase and delta-13-prostaglandin reductase) in the stomach, leading to the healing of ulcers. 29 DGL has been shown to be more cost-effective than Tagamet or Zantac, costing 85 percent less for a months supply.13
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As an aside, it should be kept in mind that modern day medicines are now able that target the Helicobacter pylori bacteria, which is a principal cause of ulcers; an effect that may not occur through the use of DGL alone (test tube studies show that DGL also kills the Helicobacter pylori bacteria, but it is not proven in-vivo). Hence, DGL may be viewed as a good complementary medicine in the treatment of peptic ulcers, in this regard. 24 Finally, a preliminary study suggests that DGL might help prevent ulcers caused by the use of aspirin and other non steroidal anti-inflammatory drugs (e.g., ibuprofen), and thus may be considered as a prophylactic intervention, by patients taking these medications for prolonged periods. 24 5. Canker Sores De-glycyrrhizinated Licorice chewable tablets may also speed the healing of apthous ulcers (canker-sores), although there is less evidence for this application than for its effects on treating and preventing peptic ulcers 14 For this purpose, DGL (200 mg) is mixed with warm water and swished in the mouth for three minutes, and then expelled. 23 (see also Reishi Mushroom Extract in this document) 6. Eczema, Psoriasis and Other Skin Conditions With topical application, glycyrrhetinic acid produces an effect similar to hydrocortisone, and has been used with some success in the treatment of eczema and psoriasis.15 An extract of Licorice, called liquiritin, has been used as a treatment for melasma, a pigmentation disorder of the skin. One study showed a 70% improvement rating when this cream was applied twice daily for four weeks, compared to only 20% improvement in the placebo group. 25 Licorice creams and gels can also be applied directly to herpes sores, and may help to speed the healing of these lesions. 25
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As a result of these common side effects, long-term use of Licorice extract or whole Licorice supplementation should only be undertaken if prescribed by a qualified health professional, who is able to monitor side effects, including certain parameters of the blood chemistry profile. 23, 29 Licorice may also interfere with hormone replacement therapy and hypoglycemic therapy. 18 It inhibits or enhances the activity of prednisone, and should not be used in conjunction with a vast number of medications, as outlined below. 1,19 The following side effects are common at doses of 400 mg or more of glycyrrhizin per day: 13 - Hypertension - Sodium and water retention - Excessive potassium excretion (hypokalemia) - Cardiac Arrhythmias - Amenorrhea - Hyperprolactemia (with possible infertility) 13 - Several deaths have resulted from the ingestion of Licorice products.1 The Dutch Nutrition Information Bureau suggest that no more than 200 mg of glycyrrhizin should be consumed daily.20 According to the German Commission E Monographs, Licorice is contraindicated in the following conditions: cholestatic liver disorders, liver cirrhosis, hypertension, hypokalemia, severe kidney insufficiency and pregnancy, as well as in cases of edema or congestive heart failure. 29
Drug-Nutrient Interactions
Licorice supplementation (excluding DGL) has been shown to cause electrolyte imbalances in some individuals and thus, its use is contraindicated in patients on the following medications: Digoxin and Digitalis 1, 18, 31,32 Laxatives 33,34 Lithium 35, 36 Licorice has also been reported to alter the effectiveness of the following drugs and thus, its use is contraindicated in patients on the following medications: Antihypertensive drugs Diuretics 37,38
37, 38
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Corticosteroid drugs (e.g., predisone): Licorice can either potentiate or inhibit the effects of predisone and other coricosteroid drugs. 35,36 Nitrofurantoin: Licorice increases the absorption and blood levels of this drug. 41 Anticoagulants: Licorice has been shown to increase risk of a bleeding disorder if taken concurrently with warfarin or coumadin. 37,38 Side Note As noted earlier, most of the Licorice candy available in North America is flavoured with anise oil, not Licorice.21 Authentic Licorice candy contains between 0.26 mg/g and 7.9 mg/g of glycyrrhizin; while medicinal Licorice products range from 0.30 mg/g to 47.1 mg/g of glycyrrhizin.22 Authors Note: Generally speaking, a number of other herbal agents can be used more safely for PMS, as antiinflammatory agents and for liver support, in place of Licorice. The most useful role of Licorice appears to be for the treatment of peptic ulcers through the use of chewable DGL tablets, which do not produce the side effects associated with other Licorice supplement products.20
1. 2. 3. 4.
Boon H and Smith M. Health Care Professional Training Program In Complementary Medicine, Institute of Applied Complementary Medicine Inc 1997:227-235. Murray MT. The Healing Power of Herbs, Rocklin CA; Prima Publishing 1992:246 Newall CA, Anderson LA, Phillipson JD. Herbal Medicines:A Guide For Health Care Professionals, London;The Pharmaceutical Press 1996:296. Kroes BH, Beukelman CJ, van den Berg AJ, Wolbink GJ, van Dijk H, Labadie RP.Inhibition of Human Complement by Beta-glycyrrhetinic Acid, Immunology 1997;90(1):115-120
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5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38.
Suzuki H, Ohta Y, Takino T, Fugisawa Kea.Effects of Glycyrrhizin on Biochemical Tests in Patients with Chronic Hepatitis: Double-blind Trial, Asian Medical Journal 1984;26:423-438 Kiso Y, Tohkin M, Hikino H, et.al., Mechanisms of Antihepatotoxic Activity of Glycyrrhizin, I. Effect on Free Radical Generation and Lipid Peroxidation, Planta Medica 1984;50:298-302 Morgan AG, McAdam WAF, Pacsoo C, Darnborough A. Comparison between Cimetidine and Caved-S in the Treatment of Gastric Ulceration, and Subsequent Maintenance Therapy, Gut 1982;23:545-551 Glick L. Deglycyrrhizinated Liquorice for Peptic Ulcer, Lancet 1982;2:p 817 Tewari SN, Wilson AK. Deglycyrrhizinated Liquorice in Duodenal Ulcer, Practitioner 1972;210:820-825 Kassir ZA. Endoscopic Controlled Trial of Four Drug Regimens in the Treatment of Chronic Duodenal Ulceration, Irish Medical Journal 1985;78:153-156 Murray M. The Healing Power of Herbs (2nd edition), Prima Publishing 1995:228-239 Das SK, Gulati AK, and Singh VP. Deglycryrrhizinated Liquorice in Aphthous Ulcers, J Assoc Physicians India 1989;37:p647 Evans FQ. The Rational Use of Glycyrrhetinic Acid in Dermatology, Br J Clin Pract 1958;12:269-279 Sharaf A and Goma N. Phytoestrogens and Their Antagonism to Progesterone and Testosterone, J Endocrinol 1965;31:289-290 Stormer FC, Reistad R, and Alexander J. Glycyrrhizic Acid in Liquorice Evaluation of Health Hazard, Fd Chem Toxicol 1993;31303-312 Biglieri EG. My Engagement with Steroids: A Review-Steroids 1995;60(1):52-58 Schleimer RP. Potential Regulation of Inflammation in the Lung by Local Metabolism of Hydrocortisone, American Journal of Respiratory Cell and Molecular Biology 1991;4:166-173 Chandler RF. Glycyrrhiza Glabra In: De Smet PAGM, Keller K, Hansel R, Chandler RF, eds, Adverse Effects of Herbal Drugs, Volume 3 ed., New York: Springer 1997:67-87 Tyler V, The Honest Herbal (3rd edition), Binghampton, New York: Pharmaceutical Products Press 1993:p375 Spinks EA, Fenwick GR. The Determination of Glycyrrhizin in Selected UK Liquorice Products, Food Additives and Contaminants 1990;7:769-778 Dietary Supplement Information Bureau. www.content.intramedicine.com:Licorice Healthnotes, Inc. 2001. www.healthnotes.com:Licorice Natural Products Encyclopedia. www.consumerslab.com:Licorice Rees, WD, Rhodes J, Wright JE et al. Effect of deglycyrrhizinated liquorice on gastric mucosal damage by aspirin. Scand J Gatroenterol 1979;14:605-7 Amer M, Metwalli M. Topical liquiritin improves melasma. Int J Dermatol 2000;39:299-301 Blumenthal M, Busse WR, Goldberg A et al. (eds.) The Complete Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, MA: Integrative Medicine Communications 1998:161-2 Bardhan KD, Cumberland DC, Dixon RA, Holdsworth CD. Clinical trial of deglycyrrhizinised liquorice in gastric ulcer. Gut 1978;19:779-82 Das SK, Das V, Gulati AD, Singh VP. Deglycyrrhizinated licorice in aphthous ulcers. J Assoc Physicians India 1989;37:p647 Mills S, Bone K. 30 Principles and Practice of Phytotherapy. Churchill Livingstone:465 478 Armanini D, Palermo M. Reduction of serum testosterone in men by licorice. N Engl J Med 1999;341:p1158 Farese RV et al. Licorice-induced hyperminarlocorticoidism. New England J Med 1991;325:1223-7 DeSmet P et al. Adverse Effects Of Herbal Drugs I. Berlin, Springer-Verlag 1992:97-104 Epstein MT et al. Effect of eating liquorice on the rennin-angiotensin-aldosterone axis in normal subjects. Br Med J 1977;1:488-90 Takeda R et al. Prolonged pseudoaldosteronism induced by glycyrrhizin. Endocrinology Japan 1979;26(5):541-7 Gibson MR. Glycyrrhiza in Old and New Perspectives. Lloydia 1978;41(4):348-54 MacKenzie MA et al. The Influence of Glycyrrhetinic Acid on Plasma Cortisol and Cortisone in healthy Young Volunteers. J Clin Endocrin Metab 1990;70:1637-43 Hatano T et al. Phenolic constituents of licorice III. Structures of glicoricone and licuforanone, and inhibitory effects of licorice constituents on monoamine oxidase. Clin Pharm Bull 1988;36:2090-7 Mahram GH et al. A further contribution to the triterpenoid constituents of glycyrrhiza glabra. Planta Medica 1989;55:p629
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5. Competitive Binding with Some Toxins: Silymarin appears to compete with amanita phalloides based toxins (from toadstool (deathcap) mushrooms) for a receptor on the cell membrane. Under experimented conditions, silymarin prevents death in animals exposed to these very lethal liver toxins when given prior to the amanita phalloides toxins, or within 10 minutes after exposure to these toxins. 10,7,8,18 6. Increased Superoxide Dismutase Concentrations: Silymarin has been shown to increase the concentrations of superoxide dismutase a very powerful intracellular antioxidant, which quenches the superoxide anion (a very 19 aggressive damaging and reactive, free radical oxygen species). Clinical Applications: (Primarily The Treatment of Various Liver Conditions) 1. Cirrhosis: Patients with liver damage due to excess alcohol consumption have shown improvement in laboratory, and liver biopsy assessment after silymarin treatment. Another study revealed improved survival in patients with cirrhosis who were treated with silymarin versus placebo, in a 4-year study involving 87 patients. 20,21,22 A doubleblind, placebo-controlled study involving 106 Finnish soldiers with alcoholic liver disease revealed that treatment with Milk Thistle produced improvement in regards to a reduction in liver enzyme blood levels and histological improvement of liver cells, as evidenced by liver biopsy samples in 29 subjects. 49 Two other studies have provided similar evidence 50, 51, although not all studies performed to date have demonstrated these types of positive results in alcoholic liver disease. 52,53 2. Chronic Viral Hepatitis and Acute Hepatitis: Most, but not all, studies have shown the effectiveness of silymarin in treating both acute and chronic hepatitis. 10,23,24,47 In the majority of these studies improvement in bilirubin levels and liver serum enzymes have been documented, and a reduction in abdominal discomfort, fatigue, and improved appetite have been reported in patients treated with silymarin. To date the majority of successful clinical trials have administered silymarin intravenously (I.V.) and therefore, the applicability of these findings to the oral ingestion of silymarin is not completely known. 10,23,24,25 However, one recently completed, well-designed clinical trial showed that the oral intake of Milk Thistle (yielding 240 mg per day) decreased blood levels of AST, ALT, and gammaglutamyltransferase (GGT) in a study of 20 patients with chronic viral hepatitis. These are all known to be important liver enzyme blood tests that are highly correlated with the degree of liver damage. 23 3. Protection from Chemical Toxins: Animal studies reveal that Milk Thistle extract protects the liver from a variety of toxins including alpha-amanitin and phalloidin (both from the extremely poisonous Deathcap or Toadstool mushroom), carbon tetrachloride, thioacetamide, DL-ethionine, phenothiazines acetaminophen and ethanol 10,26,27,28,29,47 (alcohol). Several human studies have shown that silymarin can reverse certain instances of liver damage induced by alcohol consumption (treated subjects demonstrated improved values for amino transferase (AST) and alanine aminotransferase (ALT) in blood testing). There was also a trend in the concentrations of total and conjugated 10,30 serum bilirubins in the silymarin group, compared to the controls. Another study with patients taking the psychotropic drugs phenothiazines or butyrophenones, demonstrated that silymarin decreased liver damage induced by these drugs and decreased serum levels of malondialdehyde (MDA), which is a biomarker for the production of free radicals. 31 However, a study examining the protective role of Milk Thistle in Alzheimers patients taking the drug tacrine, failed to show that Milk Thistle could prevent the liver inflammation that is known to be a side effect of this medication. 54 4. Enhance Detoxification: For general support of liver detoxification in anti-aging medicine silymarin has been shown to significantly increase liver concentrations of glutathione, increase solubility of bile and provides additional antioxidant support to liver cells. As such, it is recommended by anti-aging and holistic practitioners as supplement that may help to slow the biological processes of aging and exert a number of health-promoting effects that are consistent with principles of disease prevention practices. 10,32,11,12
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5. Psoriasis: A number of reports suggest that silymarin may be of value in the treatment of psoriasis, likely due to its ability to inhibit the synthesis of pro-inflammatory leukotrienes and improve the livers capacity to detoxify foreign compounds and contaminants. Some evidence suggests that certain bioactive agents absorbed in the intestinal tract, that escape detoxification by the liver and intestinal mucosal cells, may trigger inflammatory reactions involved in the exacerbation of skin conditions, such as psoriasis. 33,34 This application, however, requires further substantiation, according to certain authorities. 47 6. Sluggish Liver or Minor Hepatic Insufficiency: This term is usually used by European physicians and American Naturopaths to describe a myriad of symptoms involving aching beneath the ribs, fatigue, unhealthy skin appearance, general malaise, constipation, allergies, premenstrual syndrome, and/or chemical sensitivities, for which Milk Thistle has been recommended. 55
After 8-12 weeks improvement should occur, allowing a reduction to 140 mg twice per day.
34 38
Drug-Nutrient Interactions
There are no known adverse drug interactions reported for milk thistle. However, as it stimulates liver detoxification pathways it may potentially speed up the metabolism of some drugs. Thus, practitioners should closely monitor patients on concurrent medications. 42,43,44,45 Milk Thistle may reduce the liver damage or side effects of certain medications, and thus its concurrent administration with the following medications may be advisable: Acetaminophen Anesthetics Chemotherapy Clofibrate Halopersidol Metronidazole Pravastatin Tacrine43
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Foster S. Milk Thistle. Silybum marianum. Houston, TX: American Botanical Council;1997:p7 Awang D. Milk thistle. Can Pharm J 1993;422:403-4 Wagner H. Antihepatotoxic flavonoids. Plant Flavonoids in Biology and Medicine: Biochemical, Pharmacological, and SturctureActivity Relationships (Cody V, Middleton E, Harbourne jV, eds.) Alan R. Liss, New York 1986:p545-58 Adzet T. Polyphenolic compounds with biological and pharmacological activity. Herbs Spices Med Plants 1986;1:167-84 Hikino H, Kiso Y, Wagner H, Fiebig. Antihepatotoxic actions of flavanolignans from silybum marianum fruits. Planta Medica 1984;50:248-50 Wagner H. Plant constituents with antihepatotoxic activity. Natural Products as Medicinal Agents (Beal JL and Reinhard E, eds.) Hippokrates-Verlag, Stuttgart, Germany 1981 Vogel G et al. Protection against Amanita phalloides intoxication in beagles. Toxicol appl Pharm 1984;73:355-62 Vogel G et al. Studies on pharmacodynamics, site and mechanism of action of silymarin, the anti-hepatotoxic principle from Silybum marianum (L.) Gaert. Arzneimittel-Forsch 1975;25:179-85 Valenzuela A et al. Silymarin protection against hepatic lipid peroxidation induced by acute ethanol intoxication in the rat. Biochem Pharm 1985;34:2209-12 Hikino H, Kiso Y. Natural products for liver diseases. Economic and Medicinal Plant Research 1988;2:39-72 Valenzuela A, Aspillaga M, Vial S, Guerra R. Selectivity of silymarin on the increase of the glutathione content in different tissues of the rat. Planta Medica 1989;55:420-2 Campos R, Garrido A, Guerra R, Valenzuela A. Silybin dihemisuccinate protects against gluta thione depletion and lipid peroxisation induced by acetaminophen in rat liver. Planta Medica 1989;55:417-9 Fiebrich F, Koch H. Silymarin, an inhibitor of prostaglandin synthetase. Experientia 1979;35:148-50 Fiebrich F, Koch H. Silymarin, an inhibitor of prostaglandin synthetase. Experientia 1979;35:150-2 Sonnenbichler J et al. Stimulatory effect of silibinin on the DNA synthesis in partially hepatectomized rat livers: Non-response in hepatoma and othr malignant cell lines. Biochem Pharm 1986;35:538-41 Sonnenbichler J, Zetl I. Biochemical effects of the flavonolignan silibinin on RNA, protein and DNA synthesis in rat livers. Plant Flavonoids in Biology and Medicine: Biochemical, Pharmacological, and StructureActivity Relationships (Cody V, Middleton E, and Harbourne JB, eds.) Alan R. Liss, New York 1986:319-31 Magliulo P, Carosi G, Minoli L, Gorini S. Studies on the regenerative capacity of the liver in rats subjected to partial hepatectomy and treated with silymarin. Arzneimittelforschung 1973;23:161-7 Desplaces A et al. The effects of silymarin on experimental phalloidin poisoning. Arzneimittel-Forsch 1975;25:89-96
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19. Muzes G, Deak G, Land I et al. Effect of the bioflavonoid silymarin on the in vitro activity and expression of superoxide dismutase (SOD) enzyme. Acta Physiologica Hungarica 1991;78(1):3-9 20. Schopen RD, Lange OK: Therapy of hepatoses, Therapeutic use of silymarin. Med Welt 1970;21:691-8 21. Ferenci P et al. Randomized controlled trial of silymarin treatment in patients with cirrhyosis of the liver. J Hepatol 1989;9:105-13 22. Deak G et al. Immunomodulator effect of silymarin therapy in chronic alcoholic liver diseases. Orv Hetil 1990;131:p1291-2 p1295-6 23. Buzzelli G, Moscarella S, Giusti A et al. A pilot study on the liver protective effect of silybin-phosphatidylcholine complex (IdB1016) in chronic active hepatitis. International Journal of Clinical Pharmacology Tehrapy and Toxicology 1993;31(9):456060 24. Lirussi F, Okolicsanyi L. Cytoprotection in the nineties: Experience with ursodeoxycholic acid and silymarin in chronic liver disease. Acta Physiologica Hungarica 1992;80(1-4):363-7 25. Berenguer J et al. Double-blind trial of silymarin versus placebo in the tratment of chronic hepatitis. Muench Med Wochenschr 1971;119:240-60 26. Weiss RF. Herbal Medicine. Gothenburg, Sweden: Ab Areanum 1988:362 27. Hruby C. Silibinin in the treatment of deathcap fungus poisoning. Forum 1984;6:23-6 28. Faulstich II, Jahn W, Wieland T. Silybin inhibition of amatoxin uptake in the perfused rat liver. Arzneimittelforshung 1980;30(1):452-4 29. Tuchweber B, Sieck R, Trost w. Prevention of silybin of phalloidin-induced acute hepatotoxicity. Toxicology and Applied Pharmacology 1979;51:265-75 30. Salami HA, Sarna S. Effect of silymarin on chemical, functional and morphological alterations of the liver. Scandinavian Journal of Gastroenterology 1982;17:517-21 31. Palasciano G, Portincasa P, Palmieri V et al. The effect of silymarin on plasma levels of malondialdehyde in patients receiving longterm treatment with psychotropic drugs. Current Therapeutic Research 1994;55(5)537-45 32. Nassauto G et al. Effect of silibinin on biliary lipid composition. Experimental and clinical study. J Hepatal 1991;12:290-95 33. Kock HP et al. Silymarin: Potent inhibitor of cyclic AMP phosphodiesterase. Meth Find Exp Clin Pharm 1985;7:409-13 34. Weber G et al. The liver, a therapeutic target in dermatoses. Med Welt 1983;34:108-11 35. Blumenthal M, Brusse WR, Goldber A et al. The Complete German Commission E Monographs. Austin, TX: American Botanical Council 1998:p685 36. Health care professional training program in complementary medicine. Boon H and Smith M. Institute of Applied Complementary Medicine Inc. 1997:241-5 37. Wagner H et al. The chemistry of silymarin (silybin), the active principle of the fruits of silybum marianum (L.). Gaertn ArzneimForsch Drug Res 1968;18:688-96 38. Brown DJ. Herbal Prescriptions for Better Health. Rocklin, CA:Prima Publishing 1996:151-8 39. Murray MT. The Healing Power of herbs. Rocklin, CA:Prima Publishing 1992:p246 40. Brown D. Silymarin educational monograph. Townsend Newsletter for Doctors 1994;136:1282-5 41. Tyler VE. Herbs of Choice. The Therapeutic Use of Phytomedicinals. Binghamton, NY: Pharmaceutical Products Press 1994:p209 42. The Botanical Pharmacy. Quarry Health Books2000. Boon H and Smith M:250-4 43. Beckmann-Knopp S, Rietbrock S, Weyhenmeyer R et al. Inhibitory effects of silibinin on cytochrome P-450 enzymes in human liver microsomes. Pharmacol Toxicol Jun2000;86(6):2506 44. Venkataramanan R, Ramachandran V, Komoroski BJ et al. Milk Thistle, a herbal supplement, drecreases the activity of CYP3A4 and uridine disphosphoglucuronosyl transferase in human hepatocyte cultures. Drug Metab Dispos Nov2000;28(11):1270-3 45. Zhao J et al. Tissue distribution of silibinin, the major active constituent of silymarin, in mice and its association with enhancement of phase II enzymes: Implications in cancer chemoprevention. Carcinogenesis Nov1999;20(11):2101-8 46. Healthnotes Online. Healthnotes Inc, 2000. www.healthnotes.com: Milk Thistle 47. Natural Products Encyclopedia. www.consumerslab.com: Milk Thistle 48. Dietary Supplement Information Bureau. www.content.intramedicine.com: Thistle 49. Salmi HA, Sarna S. Effect of silymarin on chemical, functional and morphological alterations of the liver. A double-blind controlled study. Scand J Gastroenterol 1982;17:517-21 50. Feher J, Desk G, Muzes G et al. Liver protective action of silymarin therapy in chronic alcoholic liver diseases [in Hungarian]. Orv hetil 1989;130:2723-7 51. Fintelmann V, Albert A. Proof of the therapeutic efficacy of LegalonW for toxic liver illnesses in a double-blind trial [translated from German]. Therapiewoche 1980;30:5589-94 52. Trinchet JC, Coste T, Levy VG et al. Treatment of alcoholic hepatitis with silymarin. A double-blind comparative study in 116 patients [translated from French]. Gastroenterol Clin Biol 1989;13:120-4 53. Bunout D, Hirsch SB, Petermann MT et al. Controlled study of the effect of silymarin on alcoholic liver disease [translated from Spainch]. Rev Med Chil 1992;120:1370-5
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54. Allain H, Schuck S, lebreton S et al. Aminotransferase levels and silymarin in de novo tacrine-treated patients with Alzheimers disease. Dement Geriatr Cogn Disord 1999;10:181-5 55. Giannola C, Buogo F, Forestiere G et al. A two-center study on the effects of silymarin in pregnant women and adult patients with so-called minor hepatic insufficiency [in Italian]. Clin Ther 1985;114:129-35 56. Albrecht M, Frerick H, Kuhn U et al. Therapy of toxic liver pathologies with Legalon [in German]. Z Klin Med 1992;47:87-92 57. Adverse Drug Reactions Advisory Committee. An adverse reaction to the herbal medication in milk thistle (Silybum marianum). Med J Aust 1999;170:218-9
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Drug-Nutrient Interactions
There are no well-known drug-nutrient interactions for Muira Puama at this time.
1,4
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1. 2. 3. 4.
Duke JA. Handbook of Medicinal Herbs (Boca Raton: CRC Press) 1985 Wyanberg J. Aphrodisiacs: Contribution to the clinical validation and use of ptychopetalum guyanna (murira puama) presented at The First International Congress on Ethnopharmacology. Strasber, France June 5-9, 1990 Waynberg J, Brewer S. Effects of herbal VX on libido and sexual activity in premenopausal and postmenopausal women. Adv Ther 2000;17(5):255-62 British Herbal Pharmacopoeia. British Herbal Medicine Association. West York, England, 1983:132-133
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Picrorhiza
General Features
Picrorhiza is a perennial plant, whose roots and rhizomes have been used for thousands of years in Indian traditional medicine. It grows high in the Himalayan mountains. 1,2 Picrorhizas most important use is in the treatment and prevention of liver conditions, whereby many of its protective influences appear to be similar to those exhibited by the herb milk thistle (see milk thistle in this document). 2 It may also benefit asthma sufferers, and patients with rheumatoid arthritis or a skin condition known as vitiligo. 1,2 There have a limited number of double-blind, placebo-controlled trials performed with Picrorhiza, but several open trials have provided preliminary evidence to support the positive outcomes revealed by animal and test tube studies. As such, it is difficult to make definitive statements about its clinical use, although its long history of use in Indian traditional medicine and recently performed clinical trials indicate that it is very non toxic and is associated with only occasional mild side effects. 1,2
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Human Studies 4. Viral Hepatitis In a study of 37 patients with chonic viral hepatitis B, who received picrohriza extract and 23 patients with chronic viral hepatitis B, who received the placebo, 59% of those treated with picrohriza extract showed no sign of the viral antigen 15 to 20 days after the course of treatment. In the placebo group, only one subject demonstrated this outcome. The treatment group received a dose of 200 mg of Picrorhiza extract daily for 30 days. 10 A second clinical trail demonstrated that Picrorhiza extract, plus a variety of minerals, was also successful in treating a series of cases of acute viral hepatitis, in a study performed in India, and a number of similar reports have appeared in Indian medical literature over the years. 1,11 In a randomized, double-blind placebo controlled trial in patients diagnosed with acute viral hepatitis (HBsAG negative). Patients receiving 375 mg of Picrorhiza root powder, three times per day for 2 weeks (n= 15) demonstrated significantly lower blood levels of the liver enzymes known as SGOT, SGPT as well as bilirubin, compard to the placebo group (n= 18). In the Picrorhiza treatment group, bilirubin levels returned to normal values in 27.44 days, on average, compared to 75.9 days in the group given the placebo. 7 5. Asthma Two preliminary trials indicate that picorhiza may improve breathing ability in asthma patients and reduce the severity of the condition. 12,13 This may be related to the ablitiy of picrorohiza extract to reduce inflammation in the lungs and related air passageways. 14 However, a double-blind follow-up study failed to show a benefit in asthmatic sufferers. 15 6. Rheumatoid Arthritis Animal studies indicate that Picrorhiza extract can decrease joint inflammation. 16 A single open trial suggested that Picrorhiza extract may reduce symptoms of rheumatoid arthritis to a limited degree. 17 7. Vitiligo Picrorhiza extract appears to modulate the immune system in such a way as to produce a beneficial effect on the benign skin condition called vitiligo, which has been shown to result from a hyperactive immune system. Vitiligo is characterized by irregular, pigment-free skin patches. 18 In a preliminary trial, Picrorhiza extract, in combination with the drug methoxsalen, was shown to hasten recovery from vitiligo faster than the combination of methoxsalen and sun exposure alone. 19
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Drug-Nutrient Interactions
1. Diabetic Hypoglycemic Drugs animal studies indicate that Picrorhiza may affect blood sugar, which may alter the dose requirement of diabetic hypoglycemic medications. Thus, proper patient monitoring is advised. 20 2. Anticoagulant Drugs (warfarin, coumadin, aspirin etc.) as picrorihza has been shown in animal studies to inhibit platelet aggregation to some degree, it may potentiate the action of other anticoagulant drugs. Thus, proper patient monitoring is advised with respect to prothrombin time (INR). 14 3. Immunosuppressive Medications experimental studies indicate that Picrorhiza may stimulate the immune system and thus, may counter the effects of immunosuppressive drugs. 18,21
1. 2. 3. 4. 5. 6. 7.
Healthnotes, Inc. 2001. www.healthnotes.com: Picrorhiza Dietary Supplement Information Bureau. www.content.intramedicine.com: Picrorhiza Sabinsa Corporation product Manual: Picroliv Singh V, et al. Effect of picroliv on protein and nucleic acid synthesis. Indian J Exp Biol Jan1992;30(1):68-9 Visen PK, et al. Curative effect of picroliv on primary cultured rat hepatocytes against different hepatotoxins: an in vitro study. J Pharmacol Toxicol Methods Oct1998;40(3):173-9 Santra A et al. Prevention of carbon tetrachloride-induced hepatic injury in mice by picrorhiza kurrooa. An in vitro study. J Pharmacol Toxicol Methods Oct1998;40(3):173-9 Vaidya AB, et al. Picrorhiza kurroa (Kutaki) Royle ex Benth as a hepatoprotective agentExperimental and clinical studies. J postgrad Med Dec1996;42(4):105-8
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8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21.
Rastogi R, et al. Picroliv protects against alcohol-induced chronic hepatotoxicity in rats. Planta Med Jun 1996;62(3):283-5 Chander R, et al. Effect of picroliv on glutathione metabolism in liver and brain of mastomys natalensis infected with plasmodium berghei. Indian J Exp Biol Aug1992;30(8):711-4 Thygarajan SP, et al. Effect of Phyllanthus amcrus on chronic carriers of hepatitis B virus. The Lancet 1988 Oct1:764-6 Chaturvedi GN, Singh RH. Jaundice of infectious hepatitis and its treatment with an indigenous drug. Picrorhiza kurrooa [sic]. J Res Ind Med 1966;1:1-13 Rajaram D. A preliminary clinical trial of Picrorrhiza kurroa in brochial asthma. Indian J Pharmacol 1975;7:95-6 Shan BK, Kamat SR, Sheth UK. Preliminary report of use of Picrorrhiza kurroa root in bronchial asthma. J Postgrad Med 1977;23:118-20 Dorsch W et al. Antiasthmatic effectgs of picrorhiza kurroa: Androsin prevents allergen- and PAF-induced brochial obstruction in guinea pigs. Int Arch Allergy Appl Immunol 1991;95(2-3):128-33 Doshi VB, Shetye VM, Mahashur AA, Kamat SR. Picrorrhiza kurroa in bronchial asthma. J Postgrad Med 1983;29:89-95 Hart BA, Simons JM, Knaan-Shanzer S, et al. Antiarthritic activity of the newly developed neutrophil oxidative burst antagonist apocynin. Free Rad Biol Med 1990;9:12731 Langer JG, Gupta OP, Atal CK . Clinical trials on Picrorhiza kurroa. Ind J Pharmacol 1981;13:98103 [review] Atal CK, et al. Immunomodulating agents of plant origin I:Preliminary Screening. J Ethnopharmacol Nov1986;18(2):133-41 Bedi KL, Zutshi U, Chopra CL, Amla V. Picrorhiza kurroa, an Ayurvedic herb, may potentiate photochemotherapy in vitiligo. J Ethnopharmacol 1989;27:34752 Joy KL, et al. Anti-diabetic activity of picrorrhiza kurroa extract. J Ethnopharmacology Nov1999;67(2):143-8 Sharma ML, et al. Immunostimulatory activity of picrorhiza kurroa leaf extract. J Ethnopharmacol Feb1994;41(3):185-92
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and is often
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Clinical Studies: At least ten double-blind, clinical trials, involving more than 600 men with BPH, have shown that Pygeum extract is an effective natural agent in the treatment of this condition. Most trials lasted 45 to 90 days and results generally showed a significant reduction in nighttime urination, urinary frequency, and residual urine volume, as well as a stronger urine stream, in men with diagnosed BPH. Pygeum extract is more popular in France and Italy, than in Germany.32 The exact mechanism as to how Pygeum works is no fully understood, but it does not appear to block the conversion of testosterone to dihydrotestosterone by inhibiting the 5-alpha reductase enzyme, which is the action of the drug finesteride and likely the therapeutic action of some natural agents such as Saw Palmetto, Stinging Nettle and Genistein (soy-derived isoflavone). Rather, Pygeum is thought to reduce prostate inflammation and congestion, and has been shown to inhibit other prostate growth factors linked to BPH. 1,33,34
Drug-Nutrient Interactions
There are no well-known drug-nutrient interactions for Pygeum Africanum.
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1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35.
Murry M. The Healing Power of Herbs. Prima Publishing 1995:286-93 Muntzing J et al. Direct and indirect effect of docosanol, the active principle in Tadenan, on the rat prostate. Invest Urol 1979;17:176-80 Thieblot L. Preventive and curative action of Pygeum africanum extracts on experimental prostatic adenoma in the rat. Therapie 1975;26:575-80 Hinman F. Benign Prostatic Hyperplasia. Springer-Verlag, NY 1983 Bombardelli E. Methods, composition and compounds for the tratment of prostatic adenoma. European Patent Appl 8330491.3, June 10, 1985 Marcoli M. Anti-inflammatory and antiedemigenic activity of extract of Pygeum africanum in the rat. New Trends Androl Sci 1985;1:89 Guillemin P. Clinical trials of V1326, or Tadenan, in prostatic adenoma. Med Pract 1970;386:75-6 Lange J, Muret P. Clinical trial of V1326 in prostatic disease. Medicine 1970;11:2807-11 Wemeau L, Delmay J, Blankaert J. Tadenan in prostatic adenoma. Vie Medicale January 1980:585-8 Viollet G. Clinical experimentation of a new drug from prostatic adenoma. Vie Medicale June, 1970:3457-8 Lhez A, Leguevague G. Clinical trials of a new lipid-sterolic complex of vegetal origin in the tratment of prostatic adenoma. Vie Medicale December 1970:5399-5404 Thomas JP, Rouffilange F. The action of Tadenan in prostatic adenoma. Rev Int Serv 1970;43:43-5 Huet, JA. Prostatic disease in old age. Med Intern 1970;5:405-8 Rometti A. Medical treatment of prostatic adenoma. La provence medicale 1970;38:49-51 Gallizia F, Gallizia G. Medical treatment of benign prostatic hypertrophy with a new phytotherapeutic principle. Recent Med 1972;9:461-8 Durval A. The use of a new drug in the treatment of prostatic disorders. Minerva Urol 1970;22:106-11 \Pansadoro V, Benincasa A. Prostatic hypertrophy:Results obtained with Pygeum africanum extract. Minerva Med 1972;11:119-44 Zurita EI, Pecorini M, Cuzzoni G. Treatment of prostatic hypertrophy with Pygeum africanum extract. Rev Bras Med 1984;41:364-6 Maver A. Medical therapy of the fibrous-adematose hypertrophy of the prostate with a new vegetal substance. Minerva Med 1972;63:2126-36 Bongi G. Tadenan in the treatment of prostatic adenoma. Minerva urol 1972;24:129-39 Doremieux J, Masson JC, Bollack C. Prostatic hypertrophy, clinical effects and histological changes produced by a lipid complex extracted from Pygeum africanum. J med Strasbourg 1973;4:253-257 Del Valio B. The use of a new drug in the treatment of chornic prostatitis. Minerva Urol 1974;26:81-94 Colpi G, Farina U. Study of the activity of chloroformic extract of Pygeum africanum bark in the treatment of urethral obstructive syndrome caused by non-cancerous prostapathy. Urologia 1976;43:441-8 Donkervoort T et al. A clinical and urodynamic study of Tadenan in the treatment of benign prostatic hypertrophy. Urology 1977;8:218-25 Dufour B, Choquenet C. Trial controlling the effects of Pygeum africanum extract on the functional symptoms of prostatic adenoma. Ann Urol 1984;18:193-5 Legramandi C, Ricci-Barbini V, Fonte A. The importance of Pygeum africanum in the treatment of chronic prostatitis void of bacteria. Gaz Medica Ital 1984;143:73-6 Ranno S et al. Efficacy and tolerability in the treatment of prostatic adenoma with Tadenan 50. Progresso Medico 1986;42:165-9 Frasseto G et al. Study of the efficacy and tolerability of Tadenan 50 in patients with prostatic hypertrophy. Progresso Medico 1986;42:4952 Bassi P et al. Standardized extract of Pygeum africanum in the treatment of benign prostatic hypertrophy. Minerva Urol 1987;39:45-50 Barlet A et al. Efficacy of Pygeum africanum extract in the medical therapy of urination disorders due to benign prostatic hyperplasia: Evaluation of objective and subjective parameters. A placebo-controlled double-blind multicenter study. Wien Klin Wochenschr 1990;102:667-73 Healthnotes Online. Healthnotes Inc, 2000;www.healthnotes.com:Pygeum Natural Product Encyclopedia. www.consumerslab.com:Pygeum Andro MC, Riffaud JP. Pygeum africanum extrct for the treatment of patients with benign prostatic hyperplasia:a review of 25 years of published experience. Vurr Ther Res 1995;56:796-817 Yablonsky F, Nicolas V, Riffaud JP et al. Antiproliferative effect of Pygeum africanum extract on rat prostatic fibroblasts. J Urol 1997;157:2381-7 Bombardelli E, Morazzoni P. Prunus africana (Hook, f.)Kalkm. Fitoterapia. 1997;68:205-18
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35% of postmenopausal women use it and half of those women discontinue HRT within a year, often due to side effects such as bleeding and breast pain or because of concerns about breast or uterine cancer, and thromboembolic disease. In fact, HRT is contraindicated in about 10% of postmenopausal women, including those who have a history of estrogen-dependent malignancy (breast cancer, uterine cancer, etc.), clotting disorders associated with estrogen use or active liver or thromboembolic disease. It is interesting to note that 85% of North American women experience hot flashes and other vasomotor changes during menopause, whereas a study of menopausal Thai women revealed that only 27% of these women experience these menopausal symptoms. A study of Japanese women noted a similar finding. Researchers believe that the higher intake of isoflavones in the traditional Asian diet accounts for the lower incidence of menopausal symptoms experienced by Asian women. This is further supported by migration studies that indicate that Asian women living in North America who abandon their traditional dietary patterns have a higher incidence of chronic and degenerative diseases, including hormone-dependent cancers, colon cancer, and cardiovascular disease compared with those who consume traditional Japanese diets. Other studies have shown that postmenopausal women with higher urinary excretion of isoflavones (a marker for higher intake and higher blood levels of isoflavones) demonstrate a significant reduction in hot flashes compared to women who excrete less than 2 mg of urinary isoflavones per day, on average (in women not using HRT).7 Authors Note: At this time, it appears that soy isoflavones and black cohosh provide the most reliable relief of menopausal symptoms and are also the safest natural interventions to use, regarding contraindications, side effects and drug-nutrient interactions. (See Soy and Black Cohosh in this document) 3. Bone Density and Osteoporosis Red Clover has been evaluated for its potential ability to support bone density through the effects of its phytoestrogen content. A one year trial (double-blind, placebo-controlled) involving 107 women showed that 40 mg of Red Clover extract decreased the rate of bone mineral density loss and bone mineral content reduction in the lumbar spine in pre and peri-menopausal women. No effect was seen in the hip or in urinary bone markers. Another study found that Red Clover extract supplementation increased bone mineral density in the proximal radius and ulna. 7,8 Studies using soy have also demonstrated a positive effect on bone density as well as the use of ipriflavone, a derivative of soy isoflavones.7 4. Cholesterol Lowering A review of the scientific literature revealed that three out of four clinical trials involving postmenopausal women found that Red Clover did not reduce high cholesterol or produce any significant changes to serum lipid levels. 6,9 By comparison, evidence supports the use of soy extract and soy foods as a natural cholesterol-lowering intervention.7,10 One study did show that Red Clover extract was able to increase HDL-cholesterol by 15 to 29% and reduce serum apolipoprotein B by 11.5-17% in postmenopausal women, after six months of treatment. These findings require verification.8
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Drug-Nutrient Interactions
Anti-coagulant Medications - The high coumarin content of Red Clover lends itself to an increase risk of bleeding disorders if combined with aspirin, warfarin, coumadin, heparin, Plavix (clopidogrel), Trental (pentoxifylline), or any other blood thinner.5,11
1. 2. 3.
4. 5. 6. 7.
Mills S and Bone K. Principles and Practice of Phytotherapy. Churchill Livingstone, Publisher:54-6;67-8 Medical Post, Oct 3, 2000: Isoflavones and Menopause Dornstauder E, Jisa E, unterrieder I, Krenn L, Kubelka W, Jungbauer A. Estrongenic activity of two standardized red clover extracts (Menoflavon) intended for large scale use in hormone replacement therapy. J Steroid Biochem Mol Biol 2001 Jul; 78(1):67-75 Gower T. New answers to menopause? Health Jan/Feb2002;16(1) p76 Robb-Nicholson C. By the way, Doctor: Does red clover work? Harvard Womens Health Watch Dec2001;9(4):p7 Fugh-Berman A, Kronenberg F. Red clover (Trifolium pratense) for menopausal women: current state of knowledge. Menopause 2001 Sep-Oct;8(5):333-7 Nachtigall LE. Isoflavones in the management of menopause. Total Health Jul/Aug2001;23(4):p26
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8.
Clifton-Bligh PB, Baber RJ, Fulcher GR, Nery ML, Moreton T. The effect of isoflavones extracted from red clover (Rimostil) on lipid and bone metabolism. Menopause 2001 Jul-Aug;8(4):259-65 9. Howes JB, Sullivan D, Lai N, Nestel P, Pomeroy S, West L, et al. The effects of dietary supplementation with isoflavones from red clover on the lipoprotein profiles of post menopausal women with mild to moderate hypercholesterolaemia. Atherosclerosis 2000 Sep;152(1):143-7 10. Anthony MS, et al. Effects of soy isovlavones on atherosclerosis: potential mechanisms. Am J Clin Nutr Dec1998;68(6 Suppl):1390S-35S 11. Heck AM, DeWitt BA, Lukes Al. Potential interactions between alternative therapies and warfarin. Am J Health Syst Phar 2000 Jul 1;57(13):p1221-7;quiz p1228-30
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2. Immune System Enhancement (Bronchitis, Asthma, Allergies, Herpetic Conditions and HIV Infection) As noted above, Reishi Mushroom Extract modulates many components of the immunesystem, which in part, account for its apparent anti-tumor properties. Chronic bronchitis in the elderly has been shown to respond favorably to treatment using a concentrated Reishi Mushroom product in a trial involving 2,000 cases in China. This study demonstrated a better than 60% success rate. After several months of treatment there was a noted rise in the levels of immunoglobulin A in the sputum.10 Immunoglobulin A is the main immunoglobulin found in the respiratory tract. A deficiency is common in allergies,19 systemic lupus and rheumatoid arthritis.20 Reishi Mushroom Extract supplementation has been shown to help improve cases of asthma and allergies. Two constituents of Reishi Mushroom Extract, oleic acid and cyclooctasulfur were shown to inhibit the release of histamine, which is likely how it benefits asthmatic and allergic patients.10,21,22 A specific protein-bound polysaccharide component of Reishi Mushroom Extract known as GLhw-02 has been shown to possess potent anti-viral properties against herpes simplex virus type 1 and type-2 under experimental conditions.23 A small human trial demonstrated that Reishi Mushroom Extract reduced pain dramatically in two patients with postherpetic neuralgia and in two other patients with severe pain due to herpes zoster infection (shingles, which is caused by a herpes virus).24 Under experimental conditions, various ganoderic acids in Reishi Mushroom Extract have been shown to be active anti-HIV agents, showing an ability to reduce viral replication by 50% at conservative doses. 25 Combined with other Oriental herbs, reishi is currently used in treatments of AIDS-related complex, AIDS, and alone or in combination formulas to treat chronic fatigue syndrome.26,27,28 Finally, studies on male mice reveal that Reishi Mushroom Extract was effective in enhancing the recovery of cellular immunocompetence after gamma-ray irradiation. Reishi Mushroom supplementation significantly increased white blood cell count (leukocytes) and other parameters of immune function in these animals, 29 in a similar fashion as has been shown to occur with astragalus supplementation in patients treated with chemo- or radiation therapy. (See Astragalus in this document.) 3. Cardiovascular Health (High Blood Pressure and Reduced Platelet Aggregation) Two human controlled studies revealed that Reishi Mushroom Extract can reduce high blood pressure to a significant degree (systolic and diastolic), even in patients who had previously failed to respond to established anti-hypertensive medications.30,31 Animal studies reveal that Reishi Mushroom Extract reduces blood pressure through a central inhibition of sympathetic nerve activity, although it does not slow heart rate or induce a sedative effect in general. 32 Under experimental conditions, Reishi Mushroom Extract has a mild to moderate effect on reducing platelet aggregation, which may further help to decrease risk of cardiovascular disease. (33) It has also been shown to increase endurance, blood flow to the brain and to improve oxygenation of cells. As such, it aids energy production on a cellular level, which may improve cardiovascular health and is used to boost memory and intellectual capacity in some cultures,34 including success in a study of Alzheimers patients.35 4. Liver Protective Effects (Hepatoprotective Properties) Reishi is prescribed in China for the treatment of chronic and acute hepatitis.36 Various ganoderic acids in reishi mushrooms have strong antihepatotoxic properties,37 which under experimental conditions have been shown to protect liver cells from chemically-induced injury, including protection from the highly toxic and lethal substance, carbon tetrachloride.38,39
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Drug-Nutrient Interactions
When used at high therapeutic doses, Reishi Mushroom Extract has the potential to potentiate (enhance) the effects of the following types of medications, and thus requires proper patient monitoring: - Antihypertensive medications 43,44 - Hypoglycemic medications 45 - Anticoagulant medications (e.g. warfarin, coumadin) 46
Jong SC, et al. Medicinal benefits of the mushroom ganoderma. Adv Appl Microbiol 1992;37:101-34 Herbs to the Rescue. Nutrition News 30Nov92;V.XVI(11):p4
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3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.
Jones K. Reishi (Ganoderma): Longevity Herb of the Orient-Part 2. Townsend Letters for Doctors & Patients 20Nov92;112:1008-12 Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Foods, Drugs, and Cosmetics, 2nd ed. New York: John Wiley & Sons 1996:255-60 Hobbs C. Medicinal Mushrooms. Santa Cruz, CA., Botanica Press 1995:96-107 Ikekawa T, et al. Antitumor action of some basidiomycetes, especially phellinus linteus. Japan J Can Res 1968;59:p155157 Morishige F. Lecture 1988. In: Becoming healthy with reishi, III. Kampo I-YS, Toyo-Igaku Sha Co. Ltd. Tokyo:12-20 (trans.) Tsukagoshi S, et al. Krestin (PSK). Cancer Treat Rev 1984;11(2):131-135 Teikoku Chemical Industry Co. Ltd. 1982. Mushroom glycoproteins as neoplasm inhibitors. Japanese Patent No. 82 75,926 12May82; in Chem Abstr;97:p4431 1j Lingzhi. In Chang HM and But PP-H, eds. Pharmacology and Applications of Chinese Materia Medica, Vol I Singapore:World Scientific 1986:642-653 Nakashima S, et al.. Effect of polysaccharrides from ganoderma applanatum on immune responses I. Enhancing effect on the induction of delayed hypersensitivity in mice. Microbiol Immunol 1979;23(6):501-513 Li S-C, Pen T-S, Kang M. Shang Wu Printer, Shanghai 1933 (trans.) Liu B, Bau Y-S. Fungi Pharmacopoeia (Sinica). The Kinoko Company, Oakland, CA 1980:168-169 Lin JM, et al. Radical scavanger and antihepatotoxic activity of ganoderma formosanum, ganoderma lucidum and ganoderma neojaponicum. J Ethnopharmacol Jun 1995;47(1):33-41 Wang SY, Hsu ML, Hsu HC, Tzeng CH, Lee SS, Shiao MS, et al. The anti-tumor effect of ganoderma lucidum is mediated by cytokines released from activated macrophages and T lymphocytes. Int J Cancer 17Mar97;70(6):699-705 Lee JM, Kwon H, Jeong H, Lee JW, Lee SY, Baek SJ, et al. Inhibition of lipid peroxidation and oxidative DNA damage by Ganoderma lucidum [In Process Citation]. Phytother Res May 2001;15(3):245-9 Wang SY. The anti-tumor effect of ganoderma lucidum is mediated by cytokines released from activated macrophages and T Lymphocytes. Int J Cancer. May 1997;70(6):699-705 Sone Y, et al. Structures and antitumor activities of the polysaccharides isolated from fruiting body and the growing culture of mycelium of ganoderma lucidum. Agr Biol Chem 1985;49:2641-53. Tizard IR. Immunology:An Introduction. Saunders, Philadelphia 1984:p94;p323 Hayward AR. Immune Deficiency Disease. In Allergic Diseases from Infancy to Adulthood. Bierman C. Warren and David S. Pearlman, eds. W.B. Saunders, 2nd ed 1988:34 Tasaka T, et al. Anti-allergic constituents in the culture medium of Ganoderma lucidum (I). Inhibitory effect of oleic acid on histamine release. Agents and Actions 1988;23(3/4):153-6 Tasaka T, et al. Anti-allergic constituents in the culture medium of ganoderma lucidum (II). Inhibitory effect of cyclooctasulpher on histamine release. Agents and Actions 1988;23(3/4):157-160 Lee SY. Eo, SK, et al. Antiherpetic activities of various protein bound polysaccarides isolated from ganoderma lucidum. J Ethnopharmacol. Dec 1999;68(1-3):175-81 Hijikata Y, et al. Effect of Ganoderma lucidum on Postherpetic Neuralgia. Am J Chin Med 1998;26(3-4):375-81 el-Mekkawy S, et al. Anti-HIV-1 and Anti-HIV-1-protease substances from ganoderma lucidum. phytochemistry. Nov 1998;49(6):1651-57 Willard T., Jones K. Reishi Mushroom. Sylvan Press, Issaquah, WA 1990 Cohen M. 1988. Paths to wholeness in HIV infection:A comprehensive approach. In AIDS, Immunity and Chinese Medicine. Proceedings of the ninth annual symposium of the Oriental Healing Arts Institute, 23Oct88, Long Beach, CA. B.C. Enger and E.R. Long, eds. O.H.A.I., Long Beach, CA 1989:92-102 Pers. Comm. Dharmananda, Ph.D, Institute of Traditional Medicine, Portland, OR, March 1992 Chen WC, Hau, DM, Lee, SS. Effects of ganoderma lucidum and krestin on cellular immunoceompetnece in gamma-ray-irradiated mice. Am J Chin Med 1995;23(1):71-80 Kammatsuse K, Kajiware N, Hayashi K. Studies on Ganaderma lucidum:I. Efficacy against hypertension and side effect. Yakugaku Zasshi 1985;105:531-3 Jin H, Zhang G, Cao X, et al. Treatment of hypertension by ling zhi combined with hyptensor and its effects on arterial, arteriolar and capillary pressure and microcirculation. In:Nimmi H, Xiu RJ, Sawada T, Zheng C (eds). Microcirculatory Approach to Asian Traditional Medicine. New York:Eslevier Science 1996:131-8 Lee SY. Cardiovascular effects of mycelium extract of ganoderma lucidum:inhibition of sympathetic outflow as a mechanism of its hypotensive action. Chem Pharm Bull (Tokyo) May 1990;38(95:1359-64 Su C. Potentiation of ganodermic acid S on prostaglandin E (1)-induced cyclic AMP elevation in human platelets. Thromb Res Jul 2000;99(2):135-45 Jong SC, et al. Medicinal benefits of the mushroom ganodermal. Adv Appl Microbiol 1992;37:101-34
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35. Sahley BJ. Reishi Mushroom, Healing Herb of the Future. MMRC Health Educator Reports;31Jan97:1-2 36. Tamura T, et al. Fermentation product as food for patients with liver failure. In Chem Abstr;108(13):110853m. 37. Hirotani M, et al. Ganoderic Acids T, S and R. New triterpenoids from the cultured mycelia of ganoderma lucidum. Chem Pharm Bull
1986;134(95):2282-5
38. Gong Z, Lin Z-B. The pharmacological study of lingzhi (Ganoderma lucidum) and the research of therapeutical principle of Fuzheng
39. Lin J-M, Lin C-C, et al. Radical scavenger and antihepatotoxic activity of Ganoderma formosanum, Ganoderma lucidum and 40. 41. 42. 43.
Gonoderma neo-japonicum. J Ethnopharm 1995;47:33-41 Hobbs C. Medicinal Mushrooms. Santa Cruz, CA:Botanica Press 1995;96-107 McGuffin M, ed. et al. Botanical Safety Handbook. Boca Raton, CRC Press1997:p55 Horner WE, et al. Basidiomycete Allergens:Comparison of three ganoderma species. Allergy. Feb 1993;48 (2):110-16 Lee SY. Cardiovascular effects of mycelium extract of Ganoderma lucidum:Inhibition of sympathetic outflow as a mechanism of its hypotensive action. Chem Pharm Bull. (Tokyo) May 1990;38(50):1359-64 44. Kanmatsuse K, et al. Studies on Ganoderma lucidum. I. Efficacy against hypertension and side effects. Yakugaku Zasshi Oct 1985;105(10):942-47 45. Hikino H, et al. Mechanisms of hypoglycemic activity of Ganoderan B:A glycan of Ganoderma lucidum fruit bodies. Planta Med Oct 1999;55(5):423-8 46. Tao J, et al. Experimental and clinical studies on inhibitory effect of Ganoderma lucidum on platelet aggregation. J Tongji Med Univ 1990;10(4):240-3
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Some of these trials reveal that Saw Palmetto extract can actually shrink the size of the prostate gland, reversing prostate enlargement (exhibiting a type of anti-aging effect). 1,44 Mechanism of Action: The fatty acids and sterols (liposterolic extracts) derived from the Saw Palmetto berries appear to exert their therapeutic effects via the following mechanisms: a. Inhibit the intraprostatic conversion of testosterone to dihydrotestosterone (DHT), and inhibits DHTs intracellular binding and transport.22,23 DHT is a more potent form of testosterone, which stimulates prostate cells (and prostate cancer cells) to multiply excessively, causing the prostate to enlarge. 4 The conversion of testosterone to DHT occurs via the 5 alpha-reductase enzyme. Saw Palmetto extract is a 5 alpha-reductase inhibitor under experimental conditions (the drug finasteride works via the same mechanism). 22,24,25,26,27,28 b. Androgen Receptor Blockade: Saw Palmetto extract blocks the effect of testosterone and DHT by binding to androgen receptors (blocking access of testosterone and DHT from entering prostate cells), and has been shown to block the translocation of the cytosol androgen receptor to the nucleus (blocks the transport of the cytosol receptor to the nucleus, thus blocking the androgenic effect on the nucleus of the cell).29,30,31,32,33 Saw Palmetto extract may also reduce the number of androgen receptors in the prostate cell membrane, an action shown to be mediated through the effect of Saw Palmetto extract on the nuclear DNA of prostate cells (inhibiting the genetic expression of androgen receptor synthesis and transport to the cell surface). This effect would also minimize the degree to which androgen hormones could influence the prostate gland. 45 c. Anti-Estrogenic Effects: Higher circulating estrogens in the male body (usually due to increased abdominal fat, as fat cells convert androstenedione to estrone hormone) has been shown to potentially contribute to BPH. Estrone inhibits the hydroxylation (breakdown or detoxification) and subsequent elimination of DHT. Hence, DHT can accumulate more easily within prostate cells. Saw Palmetto extract has been shown to significantly lower cellular (cytosol) and nuclear estrogen and progesterone receptors on the prostate gland in men suffering from BPH, compared to the placebo group. In the prostate gland, progesterone receptor activation is linked to increased estrogenic activity. It has been suggested that the anti-estrogenic effect of Saw Palmetto extract is a primary feature of its therapeutic effect on reducing BPH. 33 In a double-blind placebo-controlled study, it was shown that of the 35 men suffering from BPH who were treated with Saw Palmetto extract compared to placebo, biopsies of their prostate gland demonstrated a significantly lower number of estrogen and progesterone receptors after treatment with Saw Palmetto for 3 months. This implies that Saw Palmetto extract may also exert an anti-estrogen and anti-progesterone effect by reducing the available number of these receptors within the prostate cell membrane. 48 d. Anti-Inflammatory Effects: Saw Palmetto extract has been reported to inhibit both the cyclooxygenase and lipoxygenase enzyme pathways, which may provide an anti-inflammatory effect and partial relief of BPH symptoms. The conversion of arachidonic acid to pro-inflammatory prostaglandins (PG-2 series) and other related leukotrienes and eicosanoids, is catalyzed by the cyclooxygenase and 5-lipoxygenasase enzymes. 34 e. Phytoestrogen Effect - Saw Palmetto extract has been shown to compete with endogenous estrogens for receptor 35,36 sites.
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Polycystic Ovarian Disease and Hirsutism Saw Palmetto extract appears to have both anti-androgenic and anti-estrogenic effects. This may also be beneficial in cases of polycystic ovarian disease (both for treatment and prevention of recurrence) as well as for hirsutism , in 4 women. Prostate Cancer Treatment Some recent evidence suggests that Saw Palmetto extract may be a useful complementary intervention in cases of prostate cancer. Recently the Journal of Clinical Oncology reported that a Saw Palmetto extract formulation (also containing six other Chinese herbs) was able to markedly reduce PSA (Prostate Specific Antigen) levels in patients with advanced prostate cancer (n=32). Al least an 80 percent reduction in PSA levels occurred in patients with androgen-dependent prostate cancer (26 patients attained undectable or anorchid PSA levels) and a 50 percent reduction in PSA levels occurred in the androgen independent-prostate cancer patients. This study carried out at the Memorial Sloan-Kettering Cancer Center used Saw Palmetto dosages that were approximately three to nine times higher than typically used to treat BPH.Some recent evidence suggests that Saw Palmetto extract may be a useful complementary intervention in cases of prostate cancer. Recently the Journal of Clinical Oncology reported that a Saw Palmetto extract formulation (also containing six other Chinese herbs) was able to markedly reduce PSA (Prostate Specific Antigen) levels in patients with advanced prostate cancer (n=32). Al least an 80 percent reduction in PSA levels occurred in patients with androgen-dependent prostate cancer (26 patients attained undectable or anorchid PSA levels) and a 50 percent reduction in PSA levels occurred in the androgen independent-prostate cancer patients. This study carried out at the Memorial Sloan-Kettering Cancer Center used Saw Palmetto dosages that were approximately three to nine times higher than typically used to treat BPH. Adverse reactions to these high doses included pulmonary embolism, hypertriglyceridemia, allergic reactions, leg cramps, nausea, diarrhea, impotence, loss of libido, hot flashes, breast tenderness, and enlargement. However, researchers conclude that it is generally well tolerated, but should not be routinely recommended to patients with a history of cardiovascular disease. 37
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The FDA in the United States lists Saw Palmetto as a herb of unknown safety. However, in Germany and Austria more than 90 percent of BPH cases are treated by physicians with phytonutrient formulations (most of which contain Saw Palmetto extract).1, 38,41 A systematic review of the literature reveals that Saw Palmetto extract is associated with fewer adverse treatment events than is the drug finasteride, including a 1% occurrence of erectile dysfunction versus 5% for finasteride. 7 Saw Palmetto extract does not appear to affect serum levels of testosterone, Follicle-stimulating hormone or Luteinizing hormone. 39 Clinical trials have shown that Saw Palmetto extract is essentially non-toxic. In a 3-year study, only 34 of the 435 subjects using Saw Palmetto extract reported any side effect, which most commonly was mild gastrointestinal distress. 44
Drug-Nutrient Interactions
Theoretically, Saw Palmetto extract may antagonize the effects of hormone replacement therapy and oral contraceptives in women, if they choose to use Saw Palmetto extract for polycystic ovarian disease or hirsutism. 1 However, no stated drug-nutrient interactions for Saw Palmetto exist at this time. 43, 44
1. 2. 3. 4. 5.
Newall CA, Anderson LA, phillipson JD. Herbal Medicines: A Guide for Health Care Professionals. London: The Pharmaceutical Press 1996:p296 Leung A, Foster S. Encyclopedia of Common Natural Ingredients used in Food, Drugs and Cosmetics. 2 nd ed. New york, NY: John Wiley and Sons 1996:p649 Awang DVC. Saw palmetto, African prune and stinging nettle for benign prostatic hyperplasia (BPG). Canadian Pharmaceutical Journal 1997; November:p37-44,p62 Murray MT. The healing Power of herbs. Rocklin, CA: Prima Publishing 1992:p246 Benign Prostatic Hyperplasia. Medical Post; Oct 17,2000
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6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36.
Paubert-Braquet M, Richardson FO, Servent-Saez N et al. Effect of Serenoa repens extract (Permixon) on estradiol/testosterone-induced experimental prostate enlargement in the rat. Pharmacological Research 1996;34(3-4):171-9 Ishani W et al. Serenoa repens for benign prostatic hyperplasia (Cochrane Review Abstract) nov 6 1998;medscape.com Cirillo-Marucco E, Pagliarulo A, Tritto G et al. Extract of Serenoa repens (PermiconR) in the early treatment of prostatic hypertrophy. Urologia 1983;5:1269-77 Tripodi V, Giancaspro M, Pascarello M et al. Treatment of prostatic hypertrophy with Seronoa repens extract. Medical praxis 1983;4:41-6 Greca P, Volpi R. Experience with a new drug in the medical treatment of prostatic adenoma. Urologia 1985;52:532-5 Crimi A, Russo A. Serenoa repens for the treatment of the functional disturbances of prostate hypertrophy. Medical Praxis 1983;4:47-51 Braeckman J. The extract of Seronoa repens in the treatment of benign prostatic hyperplasia: A multicentre open study. Current Therap Research 1994;55(7):776-85 Romics I, Schmitz H, Frang D. Experience in treating benign prostatic hypertrophy with sabal serrulata for one year. International Urology and Nephrology 1993;25(6):565-69 Boccafoschi, Annoscia S. Compariosn of Serenoa repens extract with placebo by controlled clinical trial in patients with prostatic adenomatosis. Urologia 1983;50:1257-68 Emili E, Lo Cigno M, Petrone U. Clinical trial of a new drug for treating hypertrophy of the prostate (Permixon). Urologia 1983;50:1042-8 Champault G, Bonnard AM, Cauquil J, Patel JC. Medical treatment of prostatic adenoma. Controlled trial: PA 109 vs. placebo in 110 patients. Annales dUrologe 1984;18:407-10 Tasc A, Barulli M, Cavazzana A et al. Treatment of obstruction in prostatic adenoma using an extract of Serenoa repens. Double-blind clinical test vs. placebo. Minerva Urologica E Nefrologica 1985;37:87-91 Vahlensieck WJ et al. Benign prostatic hyperplasia Treatment with Sabal fruit extract. A treatment study of 1,334 patients. Fortschritte der Medizin 1993;111:323-6 Pannunzio E et al. Serenoa repens in the tratment of human benign prostatic hypertrophy (BPH). Journal of Urology 1987;137:p226A Adriazola Semino m et al. Symptomatic treatment of benign hypertrophy of the prostate. Arch Esp Urol 1992;45:211-3 Carraro JC, Raynaud JP, Koch G et al. Comparison of phytotherapy (Permixon) with finasteride in the treatment of benign prostate hyperplasis: A randomized international study of 1,098 patients. Prostate 1996;29:231-40 Carilla E et la. Binding of Permixon, a new treatment for prostatic benign hyperplasia, to the cytosolic androgen receptor in the rat prostate. J Steroid Biochem 1984;20:521-3 Sultan C et al. Inhibition of androgen metabolism and binding by a liposterolic extract of Serenoa repens B in human foreskin fibroblasts. J Steroid Biochem 1984;20:515-9 Briley M, Carilla E et al. Inhibitory effect of Permixon on testosterone 5-alpha-reductase activity of rat ventral prostate. British Journal of Pharmacology 1984;83(suppl):p401 Delos S, Iehle C, Martin PM, Raynaud JP. Inhibition of the activity of basic; 5-alpha-reductase (type 1) detected in DU 145 cells and expressed in insect cells. Journal of Steroid Biochemistry and Molecular Biology 1994;48(4):347-52 Delos S, Carsol JL, Ghazarossian E et al. Testosterone metabolism in primary cultures of human prostate epithelial cells and fibroblasts. Journal of Steroid Biochemistry and Molecular Biology 1995;55(3-4):375-83 Iehle C, Delos S, Guirou O et al. Human prosatic steroid 5 alpha-reductase isoformsa comparative study of selective inhibitors. Journal of Steroid Biochemistry and Molecular Biology 1995;54(5-6):273-9 Rhodes L, Primka RL, Berman C et al. Compariosn of Finasteride (Proscar), a 5a reductase inhibitor and various commercial plant extracts in in vitro and in vivo 5a reductase inhibition. The Prostate 1993;22:43-51 El-Sheikh MM, Dakkak MR, Saddique A. The effect of permixon on androgen receptors. Acta obstetrica et Gynecologica Scandinavica 1988;67:397-9 Ravenna L, Di Silverio F, Russo MA et al. Effects of the lipiosterolic extract of Serenoa repens (Permixon) on human prostatic cell lines. Prostate 1996;29(4):219-30 Wilson JD. The pathogenesis of benign prostatic hyperplasia. American Journal of Medicine 1980;68:745-55 Carilla E, Briley M, Fauran Fea. Binding of Permixon, a new treatment for prostatic benign hyperplsia, to cytosolic androgen receptor in rat prostate. Journal of Steroid Biochemistry 1984;20:521-3 Di Silverio F et al. Evidence that Serenoa repens extract displays antiestrogenic activity in prostatic tissue of benign prostatic hypertrophy. Eur Urol 1992;21:309-14 Breu W, Hagenlocher M, Redl K et al. Anti-inflammatory activity of Sabal fruit extracts prepared with supercritical carbon dioxide, in vitro antagonists of cyclooxygenase and 5-lipoxygenase metabolism. Arzneimittelforschung 1992;42(4):547-51 Elghamry MI, Hansel R. Activity and isolated phytoestrogen of shrub palmetto fruits (Serenoa repens Small), a new estrogenic plant. Experientia 1969;25:828-9 Di Silverio F, DEramo G, Lubrano C et al. Evidence that Serenoa repens extract displays an antiestrogenic activity in prostatic tissue of benign prostatic hypertrophy patients. European Urology 1992;21:309-14
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37. Small EJ et al. Prospective trial of the herbal supplement PC-Spes in patients with progressive prostate cancer. JCO 2000;18(21):35953603 38. McPartland JM et al. Benign prostatic hyperplasia treated with saw palmetto:a literature search and an experimental case. J Am Osteop Assoc 2000;100(2):89-96 39. Casarosa C, Cosci di Coscio M, Fratta M. Lack of effects of a liposterolic extract of Serenoa repens on plasma levels of testosterone, FSH, and luteinizing hormone. Clinical Therapeutics 1988;10:585-88 40. Gerber GS et al. Saw palmetto (serenoa repens) in men with lower urinary tract symptoms: effects on urodynamic parameters and voiding symptoms. Urology 1998;51(6):1003-7 41. MacDonald A et al. Systematic review of cernilton for the treatment of benign prostatic hyperplasia. Br J Urol 1999;85:836-941 42. Sokeland J et al. A combination of Sabal and urtica extracts verus finasteride in BPH: a comparison of therapeutic efficacy in a one-year double-blind study. Urologe CA 1997;36:327-33 43. Healthnotes Online. Healthnotes Inc 2000. www.healthnotes.com: Saw Palmetto 44. Natural Product Encyclopedia. www.consumerslab.com: Saw Palmetto 45. Ravenna L et al. Effects of the lipidosterolic extract of serenoa repens (permixon) on human prostatic cell lines. Prostate 1996;29(4):21930 46. Delos S et al. Testosterone metabolism in primary cultures of human prostate epithelial cells and fibroblasts. J Steroid Biochem & Molecular Biol 1994;48(4):347-52 47. Paubert-Braquet M et al. Effect of serenoa repens extract (permixon) on estradiol/testosterone-induced experimental prostate enlargement in the rat. Pharmacol Res 1996;34(3):171-9 48. Di Silverio F et al. Evidence that serenoa repens extract displays an antiestrogenic activity in prostatic tissue of benign prostatic hypertrophy patients. European Urologv 1992;21(4):309-14 49. Wagner H et al. Immunostimulatin lactation of polysaccharides (heteroglycans) from higher plants. Arzneimittelforschung 1985;35(7):1069-75
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3. Genital Warts Oral supplementation of lentinan has been shown to significantly reduce the recurrence rate of genital warts (condyloma acuminata). A preliminary trial involving a group of men and women with genital warts found that those who took 12.5 mg of lentinan per day for two months after laser surgery, had a recurrence rate of only 10.5% as compared to 47% in the group that did not receive the lentinan.16
Drug-Nutrient Interactions
1. Immunosuppressive Medications (e.g., cyclosporin): As shiitake mushrooms and its extracts (e.g., LEM) are known to stimulate the immune system, they are contraindicated in cases where patients are taking immunosuppressive drugs.4,5 2. Didanosine: Shiitake Mushroom extract has been shown to enhance the efficacy of didanosine in HIV patients when administered intravenously, and thus should be considered for use in these cases.
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Dietary Supplement Information Bureau. Shiitake Mushroom. www.intramedicine.com. Dietary Supplement Education Alliance 2001 Healthnotes Inc. 2001. Shiitake Mushroom. www.puritan.com/healthnotes Gordon M, Bihari B, Goosby E, Gorter R, Greco M, Guralnik M, et al. A placebo-controlled trial of the immune modulator, lentinan, in hIVpositive patients: a phase I/II trial. J Med 1998;29(5-6):305-30 Suzuki H, et al. Immunopotentiating Substances in Lentinus edodes Mycelial Extract(LEM)-- Activation of Macrophage and Proliferation of Bone Marrow Cell. Nippon Shokakibyo Gakkai Zasshi. Jul1988;85(7):1430 Suzuki H, et al. Inhibition of the Infectivity and Cytopathic Effect of Human Immunodeficiency Virus by Water-soluble Lignin in an Extract of the Culture Medium of Lentinus edodes Mycelia (LEM). Biochem Biophys Res Commun. Apr1989;160(1):367-73 Li JF, et al. Study on the Enhancing Effect of Polyporus Polysaccharide, Mycobacterium Polysaccharide and Lentinan on Lymphokineactivated Killer Cell Activity in vitro. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih. Apr1996;16(4):224-26. Gordon M, et al. A Placebo-controlled Trial of the Immune Modulator, Lentinan, In HIV-positive Patients: A Phase I/II Trial. J Med. 1998;29(5-6):305-30 Miyakoshi H, Aoki T, Mizukoshi M. Acting mechanism of lentinan in humanII. Enhancement of non-specific cell-mediated cytotoxicity as an interferon inducer. Int J Immunopharmacol 1984;6:3739. Arinaga S, Karimine N, Takamuku K, et al. Enhanced induction of lymphokine activated killer cell after lentinan administration in patients with gastric carcinoma. Int J Immunopharmacol 1992;14:5359. Matsuoka H, Yano K, Seo Y, et al. Usefulness of lymphocyte subset change as an indicator for predicting survival time and effectiveness of treatment with the immunopotentiator lentinan. Anticancer Res 1995;15:22916. Miyakoshi H, Aoki T, Mizukoshi M. Acting mechanism of lentinan in humanII. Enhancement of non-specific cell-mediated cytotoxicity as an interferon inducer. Int J Immunopharmacol 1984;6:3739. Arinaga S, Karimine N, Takamuku K, et al. Enhanced induction of lymphokine activated killer cell after lentinan administration in patients with gastric carcinoma. Int J Immunopharmacol 1992;14:5359. Matsuoka H, Yano K, Seo Y, et al. Usefulness of lymphocyte subset change as an indicator for predicting survival time and effectiveness of treatment with the immunopotentiator lentinan. Anticancer Res 1995;15:22916. Matsuoka H, Seo Y, Wakasugi H, et al. Lentinan potentiates immunity and prolongs the survival time of some patients. Anticancer Res 1997;17:27516. Tari K, Satake I, Nakagomi K, et al. Effect of lentinan for advanced prostate carcinoma. Hinyokika Kiyo (Acta Urol Japon) Guangwen Y, Jianbin Y, Dongqin L et al. Immunomodulatory and therapeutic effects of lentinan in treating condyloma acuminata. CJIM 1999;5:190-2
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St. Johns wort is effective in the treatment of mild to moderate depression. 1,6,7,8,9 Symptoms of mild to moderate depression include depressed mood, lack of energy, sleep problems, anxiety, appetite disturbance, difficulty concentrating, poor stress tolerance and chronic irritability. Studies on St. Johns wort and other antidepressant drugs use the Hamilton Depression Index (HAM-D) to evaluate patient response. The HAM-D is a set of questions that can help establish the severity of depression and is a useful tool to track improvement through a rating scale system. An overview of all studies involving the use of St. Johns wort extract for mild to moderate depression reveals that it is effective in approximately 55% of cases. As with other antidepressants it usually requires up to 46 weeks to show a significant improvement in the patients symptoms. 12 St. Johns wort has been tested against placebo and against standard antidepressant drugs in a significant number of clinical trials, involving patients with mild to moderate depression. In double-blind placebo-controlled trials totaling more than 1,000 patients, St. Johns wort extract has shown that it can significantly reduce HAM-D scores when compared to placebo. 25 In one study HAM-D scores dropped by at least 50% in 70% of the subjects taking St. Johns wort (and in 24% of patients in the placebo group). 26 Not all studies have shown success however, but the same is true for prescription antidepressants that are in use today, such as sertraline, which in some studies has not shown a benefit. This is common in the area of depression where no real precise method is available to measure the benefit of an intervention, such as a blood test for a proven biomarker of disease progression or improvement. 27, 28 In general, the evidence to support the use of St. Johns wort for the treatment of mild to moderate depression appears to be as substantial as the use of other prescription drugs. 1,11,12,13,14 Short-term double-blind studies (6 8 weeks) testing St. Johns wort against fluoxetine (Prozac) demonstrated that St. Johns wort is equally, or more effective, than fluoxetine in treating patients with mild to moderate depression, and produced fewer and less severe side effects. 29,30 St Johns wort has also been shown to be as effective as sertraline (Zoloft) and imipramine in the treatment of moderate depression, in other head-to-head trials. 31,32 It should be noted once again that St. Johns wort does not represent a treatment option for severe depression, and that a study testing St. Johns wort against imipramine showed that imipramine was a more effective treatment for patients presenting with severe depression. 15 2. Anxiety and Insomnia In many of the studies testing St. johns wort as a treatment for depression, many patients reported an improvement in anxiety and insomnia, associated with their depression. 12,14 3. Seasonal Affective Disorder (SAD) One small controlled trial showed that St. Johns wort was effective in the treatment of SAD. 33 This may be due to its ability to raise brain levels of serotonin. Further studies are required to substantiate this preliminary report. 34 4. Viral Infections St Johns wort demonstrates antiviral activity against herpes simplex type 1 and 2, influenza A and B and vesicular stomatitis virus. Thus, it may have application for patients with these problems, although no concrete statements can be made at this time.4,5
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Drug-Nutrient Interactions
Antidepressant drugs: St. Johns wort acts in the body like many other antidepressant drugs, and has been shown to potentiate their effects, producing dangerous and severe side effects. It is therefore recommended that patients not take St. Johns wort concurrently with any other antidepressants, including the following: - 5-hydroxytryptophan 43 - Serotonin re-uptake inhibitors (SSRIs) 44-50 - MAO-inhibitors 44-50 - Tricyclic antidepressants 44-50 - Resperine 51 - Barbituates and sedatives 51
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- Any attempt combine the use of St Johns wort with an antidepressant medication should be supervised by a physician, trained in this area.11 Medications that Cause Sun Sensitivity: St. Johns wort may increase the potential for certain medications such as Sulfa drugs, Feldene and Prevacid to produce photosensitivity reactions, resulting in a severe skin rash. This is most important for fair-skinned individuals, who are most vulnerable. In these cases, sun light exposure to the skin must be limited. 12 Alters the Rate of Detoxification of Other Drugs: St. Johns wort has been shown to alter the rate of detoxification of other drugs thereby altering their dose requirement and in cases where the therapeutic safety index is very narrow, as is the case with digitalis or digixon. These drug-nutrient interaction can potentially be very dangerous. Evidence of this nature exists to suggest that St. Johns wort should not be taken concurrently with the following drugs: - Digoxin and digitalis 52 - Theophylline 53 - Immunosuppressive drugs ( e.g., cyclosporin) 54 - Oral contraceptives- where it has caused breakthrough bleeding 55,56 - Anesthetic drugs- refrain form taking St. Johns wort seven days prior to surgery 57 - Protease inhibitors 58 - Hormone replacement therapy 55 Warfarin and Coumadin 56
1. 2. 3.
Boon H and Smith M, Health Care Professional Training Program in Complementary Medicine, Institute of Applied Complementary Medicine Inc., 1997. Suzuki O, et.al., Inhibition of Monoamine Oxidase by Hypericin, Planta Medica 50, 1984, 272-274. Holtz J, Demisch L, and Gollnick B, Investigations About Antidepressive and Mood Changing Effects of Hypericum Performatum, Planta Medica 55, 1989, 643.
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4. 5.
6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32.
Schmidt U and Sommer H, St. Johns Wort Extract in the Ambulatory Therapy of Depression. Attention and Reaction Ability are Preserved, Forschr Med 111, 1993, 339-342. Johnson D, Effects of St. Johns Wort Extract Jarsin. Paper Presented at the 4 th International Congress on Phytotherapy, Munich, Germany, September 10-13, 1992. [Abstract SL53]; Woelk H, Multicentric Practice Study Analyzing the Functional Capacity in Depressive Patients, Paper Presented at the 4th International Congress on Phytotherapy, Munich, Germany, September 10-13, 1992 [Abstract SL54]; Sommer H, Improvement of Phychovegetative Complaints by Hypericum, Paper Presented at the 4 th International Congress on Phytotherapy, Munich, Germany, September 10-13, 1992 [Abstract SL55] Schlich D, Brauckmann F, and Schenk N, Treatment of Depressive Conditions with Hypericum, Psychol 13, 1987, 440-444 Harrer G and Sommer H, Treatment of Mild/Moderate Depressions with Hypericum, Phytomed 1, 1994, 3-8 Lavie D, Antiviral Pharmaceutical Compositions Containing Hypericin or Pseudohypericin, European Patent Application No. 87111467.4, filed 8/8/87, European Patent Office, Publ. No. 0 256 A2. 1987, 175-177 Someya H, Effect of a Constituent of Hypericin Erectum on Inection and Multiplication of Epstein-Barr Virus, J Tokyo Med Coll 43, 1985, 815-826 Gulick R, et.al., Human Hypericism: A Photosensitivity Reaction to Hypericin (St. Johns Wort), Int Conf AIDS 8, B90, 1992. [Abstract PoB 3018] Murray MT, The Healing Power of Herbs (2nd edition), Prima Publishing, 1995 Natural Products Encyclopedia. www.consumerslab.com:St Johns Wort Healthnotes, Inc. 2001. www.healthnotes.com:St. Johns Wort Dietary Supplement Information Bureau. www.content.intramedicine.com: St. Johns Wort Vorbach EU, Arnoldt KH, Hubner WD. Efficacy and tolerability of St. Johns Wort extract LI 160 versus imipramine in patients with severe depressive episodes versus imipramine in patients with severe depressive episodes according to ICD-10. Pharmacopsychiatry 1997;30(suppl 2):81-5 DeMott K. St. Johns wort tied to serotonin syndrome. Clinical Psychiatry News 1998;26:p28 Gordon JB. SSRIs and St. Johns wort: Possible toxicity? Am Fam Physician 1998;57:p950, p953 Lantz MS, Buchalter E, Giambanco V. St Johns wort and antidepressant drug interactions in the elderly. J Geriatr Psychiatry Neurol 1999;12:7-10 Holzl J, Demisch L, Gollnik B. Investigations about antidepressive and mood changing effects of Hypericum perforatum. Planta Med 1989;55:643. Chatterjee SS, Koch E, Noldner M, et al. Hyperforin with hypericum extract: Interactions with some neurotransmitter systems. Quart Rev Nat Med 1997;Summer:110. Calapai G, Crupi A, Firenzuoli F, et al. Effects of Hypericum perforatum on levels of 5-hydroxytryptamine, noradrenaline and dopamine in the cortex, diencephalon and brainstem of the rat. J Pharm Pharmacol 1999;51:7238. Schrader E. Equivalence of St Johns wort extract (Ze 117) and fluoxetine: a randomized, controlled study in mild-moderate depression. Int Clin Psychopharmacol 2999;15:61-8 Schrader E, Meier B, Brattstrom A. Hypericum treatment of mild-moderate depression in a placebo-controlled study: a prospective, double-blind, randomized, placebo-controlled, multicentre study. Hum Psychopharmacol 1998;13:163-9 Mller WE, Rolli M, Schfer C, Hafner U. Effects of hypericum extract (LI 160) in biochemical models of antidepressant activity. Pharmacopsychiatry 1997;30(suppl):1027 Kalb R, Trautmann-Sponsel RD, Kieser M. Efficacy and tolerability of hypericum extract WS 5572 versus placebo in mildly to moderately depressed patients. A randomized double-blind multicenter clinical trial. Pharmacopsychiatry 2001;34:96-103 Hansgen KD, Vesper J. Antidepressant efficacy of a high-dose hypericum extract [translated from German]. MMW Munch Med Wochenschr 1996;138:29-33 Shelton RC, Keller MB, Gelenberg A, et al. Effectiveness of St. Johns wort in major depression: a randomized controlled trial. JAMA 2001;285:1978-86 Hypericum Depression Trial Study Group. Effect of Hypericum perforatum (St. Johns wort) in major depressive disorder: a randomized controlled trial. JAMA 2002;287:1807-14 Schrader E. Equivalence of St Johns wort extract (Ze 117) and fluoxetine: a randomized, controlled study in mild-moderate depression. Int Clin Psychopharmacol 2000;15:61-8 Harrer G, Schmidt U, Kuhn U, et al. Comparison of equivalence between the St. Johns wort extract LoHyp-57 and fluoxetine. Arzneimittelforschung 1999;49:289-96 Brenner R, Azbel V, Madhusoodanan S, et al. Comparison of an extract of hypericum (L1 160) and sertraline in the treatment of depression: a double-blind, randomized pilot study. Clin Ther 2000;22:411-9 Philipp M, Kohnen R, Hiller KO. Hypericum extract versus imipramine or placebo in patients with moderate depression: randomized multcentre study of treatment for eight weeks. BMJ 1999;319:1534-9
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33. Martinez B, Kasper S, Ruhrmann S, et al. hypericum in the treatment of seasonal affective disorders. J Geriatr Psychiatr Neurol 1994;7(suppl 1):S29-33 34. Muller WEG, et al. Effects of Hypericum Extract on the Expression of Serotonin Receptors. J Geriatric Psychiatry and Neurology. 1994;7:S63-S64 35. Rayburn WF, Gonzalez CL, Christensen HD, et al. Effect of prenatally administered hypericum (St Johns wort) on growth and physical maturation of mouse offspring. Am J Obstet Gynecol 2001;184:191-5 36. Woelk H, Burkard G, Grunwald J. Benefits and risks of the hypericum extract LI 160: Drug monitoring study with 3,250 patients. J Geriatr Psychiatr neurol 1994;7(suppl 1):S34-8 37. Hubner WD, Arnoldt KH. St Johns wort: a one year treatment study [in German; English abstract]. Z Phytother 2000;21:306-10 38. Schulz V, Hansel R, Tyler VE. Rational Thytotherapy: A Physicians Guide to Herbal Medicine. 3 rd ed. Berlin, Germany: Springer-Verlag 1998:p56 39. De Smet PA, Nolen WA. St. Johns wort as an anti-depressant. BMJ 1996;3:241-2 40. Suzuki O, Katsumata Y, Oya M, et al. Inhibition of monoamine oxidase by hypericin. Planta Med 1984;50:272-4 41. Bladt S, Wagner H. Inhibition of MAO by fractions and constitutents of hypericum extract. J Geriatr Psychiatr Neurol 1994;7(suppl 1):S579 42. Thiede HM, Walper A. Inhibition of MAO and COMT by hypericum extracts and hypericin. J Geriatr Psychiatr Neurol 1994;7(suppl 1):S546 43. Kahn RS, et al. L-5-hydroxytryptophan in the treatment of anxiety disorders. J Affect Disord Mar1985;8(2):197-200 44. Muller WE, et al. Effects of Hypericum Extract (LI 160) in Biochemical Models of Antidepressant Activity. Pharmacopsychiatry. 1997;30(Supp 2):102-07 45. Linde K, et al. St. John's Wort for Depression--An Overview and Meta-analysis of Randomised Clinical Trials. BMJ. 1996;313m:253-58 46. Demott K. St. Johns Wort Tied to Serotonin Syndrome. Clin Psychiatry News 1998;26:28. 47. Suzuki O, et al. Inhibition of Monoamine Oxidase by Hypericin. Planta Medica 1984;50:272-74. 48. Bladt S, et al. Inhibition of MAO by Fractions and Constituents of Hypericum Extract. J Geriatric Psychiatry and Neurology 1994;7:S57S59 49. Gordon JB. SSRIs and St.John's Wort: possible toxicity? Am Fam Physician Mar1998;57(5):950,953 50. Lantz MS, Buchalter E, Giambanco V. St. John's wort and antidepressant drug interactions in the elderly. J Geriatr Psychiatry Neurol 1999;12(1):7-10. 51. Okpanyi SN, et al. Animal experiments on the psychotropic action of a hypericum extract. Arzneimittelforschung Jan1987;37(1):10-3 52. Johne A et al. Pharmacokinetic interaction of digoxin with an herbal extract from St Johns wort (Hypericum perforatum) Clin Pharmacol Ther Oct1999;66(4):338-45 53. Nebel A, et al. Potential metabolic interaction between St. Johns wort and Theophylline. Ann Pharmacother Apr1999;33(4):p502 54. Ruschitzka F, et al. Acute heart transplant rejection due to St. Johns wort. Lancet Feb2000;355(9203):548-9 55. Rey JM, et al. Hypericum perforatum (St John;s Wort) in depression: Pest or blessing? Med J Aust Dec1998;169(11-12):583-6 56. Yue Qy, Bergquist C, Gerden B. Safety of St. Johns wort (Hypericum perforatum), correspondence. Lancet 2000;355:576-7 57. Ernst E. Second thoughts about safety of St Johns Wort. Lancet Dec1999;354(9195):2014-6 58. Piscitelli SC, et al. Indinavir concentrations and St. Johns Wort. Lancet Feb2000;355(9203):547-8 59. Mills S, Bone K. Principles and Practice of Phytotherapy. Churchill Livingstone 2000:548-9
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A number of open studies involving at least 15,000 men, although less reliable than double-blind placebo controlled studies, have also shown Nettle extract to be useful in the treatment of symptoms associated with BPH. 2. Hayfever (allergic rhinitis) A small study of 69 subjects demonstrated that Nettle supplementation reduced hayfever symptoms to a significant degree, under double-blind, placebo-controlled conditions. 25 3. Arthritis A small double-blind study, along with historical use of Nettle, suggests that by applying Stinging Nettle leaf topically over arthritic joints, symptoms of pain, swelling and stiffness may improve. 26
Drug-Nutrient Interactions
There are no well-known drug nutrient interactions for stinging Nettle. Theoretically, Nettle may potentiate the effect of antihypertensive drugs and antagonize the effects of oral hypoglycemic drugs in type II diabetics, and possibly interact with sedative medications, but no clinical evidence exists to establish these interactions as a contraindication to the use of Urtica dioica at this time. 20,22
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1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.
Leung A, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. New York, NY: John Wiley and Sons 1996:p649 ESCOP. Urticae Radix/Nettle Root. In: ESCOP Monographs (Fascicule 2) Exeter: ESCOP 1996:p58 ESCOP.Urticae Folium/Herba (Nettle Leaf). In: ESCOP Monographs (Fascicule 4) Exeter: ESCOP 1997:p58 Weiss RF. Herbal medicine. Beaconsfield, England: Beaconsfield Publishers Ltd 1988:p362 Dreikorn K, Schonhofer P. Status of phytotherapeutic drugs in the treatment of benign prostatic hyperplasia. [German] Urologe A 1995;34(2):119-29 Buck A. Phytotherapy for the prostate. British Journal of urology 1996;78:325-36 Chrubasik S, Enderlein W, Bauer R, Grabner W. Evidence for antirheumatic effectiveness of herba urticae dioicae in acute arthritis: A pilot study. Phytomedicine 1997;4(2):105-8 Rand J. pilot study indicates that tewed herba urticae diocae may potentiate the effects of diclofenac in acute arthritis. Focus on Alternative and Complementary Therapies 1997;2(4):156-7 The Botanical Pharmacy. Quarry Health Books 1999. Boon H and Smith M:256-9 Schneider HJ, Honold E, Mashur T. Treatment of benign prostatic hyperplasia. Results of a surveillance study in the practices of urological specialists using a combined plant-based preparation. Forschritte der Medizin 1995;113:37-40 Harmann R, Mark M, Soldati F. Inhibition of 5 alpha reductase and aromatase by PHL-00801 (Prostatonin), a combination of PY102 (Pygeum africanum) and UR102 (Urtica dioica) extracts. Phytomedicine 1996;3(2):121-8 Belaiche P et al. Clinical studies on the palliative tratment of prostate adenoma with extract of urtica root. Phytother Res 1991;5:267-9 Romics I. Observations with Bazotion in the management of prostatic hyperplasia. Int Urol Nephrol 1987;19(3):293-7 Wagner H et al. Search for the anti-prostatic principle of stinging nettle (urtica dioica) roots. Phytomedicine 1994;1:213-24 Hyrb D, Khan M, Romas N, Rosner W. The effect of extracts of the roots of the the stinging nettle (Urtica dioica) on the interaction of SHBG with its receptor on human prostatic membranes. Planta Medica 1995;61:31-2 Konrad L et al. Antiproliferative effect on human prostate cancer cells by a stinging nettle root (urtica dioica) extract. Planta med 2000;66(1):44-7 Lichius JJ et al. Antiproliferative effect of a polysaccharide fraction of a 20% methanolic extract of stinging nettle roots upon epithelial cells of the human prostate (LNCaP) Pharmzie 1999;54(10):768-71 Pizzorno J, Murray M. Encyclopedia of Natural Medicine (2nd ed) Prima Health 1998:p762 Benign Prostatic Hyperplasia. Medical Post. Oct 17, 2000
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20. Newall C, Anderson L, Phillipson J. herbal medicines: A Guide for health Care professionals. London: The Pharmaceutical Press 1996:p296 21. Healthnotes, Inc 2001. www.healhnotes.com: nettle 22. Natural Products Encyclopedia. www.consumerslab.com: nettle 23. Dietary Supplement Information Bureau. www.content.intramedicine.com: Stinging Nettle 24. European Scientific Cooperative on Phytotherapy. Urticae radix. Exeter, UK: ESCOP, 1996-1997:4-5. Monographs on the uses of plant drugs, fascicule 2. 25. Mittman P. Randomized, double-blind study of freeze-dried Urtica dioica in the treatment of allergic rhinits. Planta Med 1990;56:44-7 26. Randall C, Randall H, Dobbs F et al. Randomized controlled trial of nettle sting for the treatment of base-of-thumb pain. J R Soc Med 2000;93:305-9 27. Shulz V, Hansel R, Tyler VE. Rational Phytotherapy: A Physicians Guide to Herbal medicine. 3 rd ed. Berlin, Germany: Springer-Verlag 1998:201-2
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Drug-Nutrient Interactions
There are no well-known drug-nutrient interaction for tribulus terrestris. Authors Note: It is probably wise to not take it concurrently with other vasodilating agents such as nitroglycerine or sildenofil (viagra).
1. 2. 3. 4. 5. 6. 7. 8.
Arcasoy HB, et al. Effect of tribulus terrestris L. saponins mixture on smooth muscle preparations: a preliminary study. Boll Chim Farm 1998;137(11):473-5 Adaikan PG, et al. Proerectile pharmacological effects of tribulus terrestris extract on the rabbit corpus cavernosum. Ann Acad med Singapore 2000;29(1):22-6 Adimoelja A. Phytochemicals and the breakthrough of traditional herbs in the management of sexual dysfunctions. Int J Androl 2000;23(suppl 2):82-4 Selected Medicinal Plants of India. Chemexil 1992:323-5 Mahato S, et al. J Chem Soc, Perkin Trans 1981;1:2405 Wright J. Muscle and Fitness. Sept 1996;p140-2,p224 Brown GA, et al. Effects of anabolic precursors on serum testosterone concentrations and adaptations to resistance training in young men. Int J Sport Nutr Exerc Metab 2000;10(3):340-59 Wang B, et al. 406 cases of angina pectoris in coronary heart disease treated with saponins of tribulus terrestris. Zhong Xi Ti Jie he Z|a Zhi 1990;10(2):85-7
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Turmeric (Curcumin)
General Features
Turmeric is a member of the ginger family. It has been used historically as a major ingredient in curry powder (flavour) and for colouring (i.e. preparation of mustard). The medicinal portions of Turmeric are the primary and secondary rhizomes. It is used medicinally in both traditional Chinese medicine and in the traditional medicine of India; primarily as a treatment for a variety of inflammatory conditions and some other health problems. Turmeric contains 0.3-5.4 percent Curcumin content, which has been shown to be a primary active constituent for medicinal purposes. As such, standardized extracts of Turmeric have been developed that are in the range of 90-95 percent Curcumin content. These products delivery a considerable amount of Curcumin at doses much lower than would be required if a patient were to use Turmeric supplementation for an intended health purpose. 1,2
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In vitro experiments have shown that Curcumin may inhibit the growth of estrogen positive human breast MCF-7 cells induced by a variety of carcinogens. This effect appears to be synergistic in combination with the soy isoflavonoid genistein.11
Drug-Nutrient Interactions
Warfarin and Coumadin: Curcumin has been shown to inhibit cyclooxygenase enzyme in platelets, reducing platelet coaguability and has demonstrated fibrinolytic effects.5,14 For these reasons it is believed that it may potentiate the anticlotting effects of warfarin or coumadin, increasing the risk of a bleeding disorder, at a high dosage. There are no adverse events of this nature reported to date, but caution is recommended at this time. 15
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1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33.
Leung A. Encyclopedia of Common Natural Ingredients Used in Food, Drugs, and Cosmetics. John wiley & Sons, New York 1980:p313-4 Ammon HPT, Wahl MA. Pharmacology of Curcuma longa. Planta Medica 1991;57:1-7 Sharma OP. Antioxidant properties of curcumin and related compounds. Biochem Pharmacol 1976;25:1811-25 Srivastava R. Inhibition of neutrophil response by curcumin. Agents and Actions 1989;28:298-303 Ammon HP, Safayhi H, Mack T, Sabieraj J. Mechanism of anti-inflammatory action sof curcumine and boswellic acids. Journal of Ethnopharmacology 1993;38(2-3):113-9 Selvam R, Subramanian L, Gayathri R, Angayarkanni N. The antioxidant activity of turmeric (Curcuma longa). Journal of Ethnopharmacology 1995;47(2):59-67 Osawa T, Sugiyama Y, Inayoshi M, Kawakishi S. Antioxidative activity of tetrahydrocurcuminoids. Bioscience Biotechnology and Biochemistry 1995;59(9):1609-12 Deodhar SD, Sethi R, Srimal RC. Preliminary studies on antirheumatic activity of curcumin (di-feruloyl methan). Indian Journal of Medical Research 1980;71:632-4 Satoskar RR, Shah SJ, Shenony SG. Evaluation of anti-inflammatory property of curcumin (di-feruloyl methane) in patients with postoperative inflammation. International Journal of Clinical Pharmacology Therapy and Toxicology 1986;24:651-4 Grant K, et al. Alternative Therapies: Turmeric. Am J Health-System Pharmacy 2000;57(12):1121-2 Verma SP, Salamone E, Goldin B. Curcumin and genistein, plant natural products, show synergistic inhibitory effects on the growth of human breast cancer MCF-7 cells induced by estrogenic pesticides. Biochemical and Biophysical Research Communications 1997;233(3):692-6 Shankar TNB, Shantha NV, Ramesh HP, et al. Toxicity studies on tumeric (Curcuma longa): Acute toxicity studies in rats, guinea pigs, and monkeys. Indian Journal of Experimental Biology 1980;18:73-5 Tyler VE. Herbs of Choice. The Therapeutic Use of Phytomedicinals. Binghampton NY: Pharmaceutical Products Press 1994:p209 Ammon HP, et al. Mechanism of anti-inflammatory actions of curcumine and boswellic acids. J Ethnopharmacol 1993;38(2-3):113-9 Heck A, et al. Potential interactions between alternative therapies and warfarin. Am J Health-Syst Pharm 2000;57(13):1221-7 Srivastava KC, et al. Curcumin, A major component of food spice turmeric (curcuma longa) inhibits aggregation and alters eicosanoids metabolism in human blood platelets. Prostaglandins Leukot Essent Fatty Acids. Apr1995;52(4):223-7 Srivastava V, et al. Effect of curcumin on platelet aggregation and vascular prostacyclin synthesis. Arzneim Forsch/Drug Res 1986;36:715-7 Healthnotes, Inc 2001. www.healthnotes.com: Turmeric Natural Products Encyclopedia. www.consumerslab.com: Turmeric Dietary Supplement Information Bureau. www.content.intramedicine.com: Turmeric Ammon HP, et al. Mechanism of anti-inflammatory actions of curcumin and boswellic acids. J Ethnopharmacol 1993;38:p113 Srivastava V, et al. Effect of curcumin on platelet aggregation and vascular prostacyclin synthesis. Arzneim Forsch/Drug Res 1986;36:715-7 Arora RB, Basu N, Kapoor V, Jain AP. Anti-inflammatory studies on Curcuma longa (turmeric). Ind J Med Res 1971;59:128995 Sreejayan N, Rao MNA. Free radical scavenging activity of curcuminoids. Arzneimittelforschung 1996;46:16971 Ramirez-Bosc A, Soler A, Gutierrez MAC, et al. Antioxidant curcuma extracts decrease the blood lipid peroxide levels of human subjects. Age 1995;18:1679 Srivastava R, Dikshit M, Srimal RC, Dhawan BN. Anti-thrombotic effect of curcumin. Thromb Res 1985;40:4137 Mehta K, et al. Antiproliferative effect of curcumin (diferuloylmethane) against human breast tumor cell line. Anticancer Drugs Jun1997;8(5):470-81 Kawamori T, et al. Chemopreventive effect of curcumin, a naturally occurring anti-inflammatory agent, during the promotion/progression stages of colon cancer. Cancer Res Feb1999;59(3):597-601 Menon LG, Kuttan R, Kuttan G. Anti-metastatic activity of curcumin and catechin. Cancer Lett 1999;141:15965 Thamlikitkul V, Bunyapraphatsara N, Dechatiwongse T, et al. Randomized double blind study of Curcuma domestica Val. For dyspepsia. J med Assoc Thai 1989;72:613-20 Rasyid A, Lelo A. The effect of curcumin and placebo on human gall-bladder function: an ultrasound study. Aliment Pharmacol Ther 1999;13:245-9 Lal B, Kapoor AK, Asthana OP, et al. Efficacy of curcumin in the management of chronic anterior uveitis. Phytotherapy Res 1999;13:31822 Soni KB, et al. Effect of oral curcumin administration on serum peroxides and cholesterol levels in human volunteers. Indian j Physiol Pharmacol Oct1992;36(4):273-5
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34. Deshpande S, et al. Subchronic oral toxicity of turmeric and ethanolic turmeric extract in female mice and rats. Toxicology Letters 1998;95:183-93 35. Kandarkar SV, Sawant SS, Ingle AD, et al. Subchronic oral hepatotoxicity of turmeric in mice-histopathological and ultrastructural studies. Indian J Exp Biol Jul1998;36(7):675-9
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Drug-Nutrient Interactions
There are no well known drug-nutrient interactions for Uva Ursi at this time. 4,8
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1. 2. 3. 4. 5.
6. 7. 8.
Leung A. Encylclopedia of common natural ingredients used in food, drugs, and cosmetics. New York: New York. John Wiley & Sons 1980:316-7. Merck Index. 10th Ed. Rahway, NJ. Merck & Co. 1983:796-7, 4721. Boon H and Smith M. The Botanical Pharmacy. Quarry Health Books. 1999: 304-307 Healthnotes, Inc. 2001 www.healthnotes.com: Uva ursi Matsuda H, Nakamura S, Tanaka T, Kubo M. Pharmacological studies on leaf of Arctostaphylos uva-ursi (L) Spreng. V. Effect of water extract from Arctostaphylos uva-ursi (L) Spreng (bearberry leaf) on the antiallergic and antiinflammatory activities of dexamethasone ointment. J Pharm Soc Japan 1992;112:673-7 Natural Products Encyclopedia. www.consumerslab.com: Uva ursi Blumenthal M, Busse WR, Goldberg A, et al. (eds.) The Complete Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, MA: Integrative Medicine Communications 1998:224-5 Dietary Supplement Information Bureau. www.content.intramedicine.com: Uva ursi
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Anxiety Several preliminary studies indicate that Valerian may be an effective treatment in cases of uncomplicated anxiety (not linked to major depression) and it has been used for this problem historically and clinically, although more research is needed to better understand its application in this regard. 1,2,3,17 Dosage and Standardized Grade Insomnia: As a mild sedative, Valerian may be taken 30-45 minutes before retiring at the following dosage and standardized grade: Valerian extract, 200 400 mg (standardized to 0.8% valerenic acids content) 8,11 Anxiety and Stress Reduction: 200 mg, twice per day (standardized to 0.8% valerenic acids content). 11
Drug-Nutrient Interactions
Valerian may potentiate the actions of the following medications and thus, it is considered to be prudent to not take Valerian concurrently with these drugs:
26 30,31,32
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1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.
Houghton PJ. The biological activity of Valerian and related plants. J Ethnopharmacol 1988;22(2):121-42. Leathwood P, et.al.. Aqueous extract of Valerian root (Valeriana Officinalis L.) Improves sleep quality in man. Pharmacol Biochem Behav 1982;17:65-71. Bakderer G, Borbely AA. Effect of Valerian on human sleep. Pharmacol 1985;87:406-9. Leathwood PD, Chauffard F. Aqueous extract of Valerian reduces latency to fall asleep in man. Planta Medica 1985;54:144-8. Lindahl O, Lindwall L. Double blind study of a Velerian preparations. Pharmacol Biochem Behav 1989;32(4):1065-6. Dressing H, et.al.. Insomnia: are Valeriana/Melissa combinations of equal value to Benzodiazepine? Therapiewoche 1992;42:726-36. Leung A. Encyclopedia of common natural ingredients used in food, drugs, and cosmetics. New York, New York. John Wiley & Sons, 1980. Murray MT. The healing power of herbs. 2nd ed. Prima Publishing, 1995. Natural Products Encysclopedia www.consumerslab.com: Valerian Healthnotes, Inc. 2001 www.healthnotes.com: Valerian Dietary Supplement Information Bureau. www.content.intramedicine.com: Valerian Mennini T, Bernasconi P, Bombardelli E, et al. In vitro study on the interaction of extracts and pure compounds from Valeriana officinalis roots with GABA, benzodiazepine and barbiturate receptors. Fitoterapia 1993;64:291300 Vorbach EU, Gortelmeyer R, Bruning J. Therapy for insomniacs:effectiveness and tolerance of valerian preparations [translated from German]. Psychopharmakotherapie 1996;3:109-15 Kamm-Kohl AV, Jansen W, Brockmann P. Modern valerian therapy for nervous disorders in old age [translated from German]. Med Welt 1984;35:1450-4 Dorn M. Efficacy and tolerability of Baldrian versus oxazepam in non-organic and non-psychiatric insomniacs: a randomized, doubleblind, clinical, comparative study [translated from German]. Forsch Komplementarmed Klass Naturkeilkd 2000;7:79-84 Schmitz M, Jackel M. Comparative study for assessing quality of olife of patients with exogenous sleep disorders (temporary sleep onset and sleep interruption disorders) Kohnen R, Oswald WD. The effects of valerian, propranolol, and their combination on activation, performance and mood of healthy volunteers under social stress conditions. Pharmacopsychiatry 1988;21:447-8 Hendriks H, Bos R, Woerdenbag HJ, et al. Central nervous depressant activity of valerenic acid in the mouse. Planta Med 1985;1:28-31 Leuschner J, Muller J, Rudmann M. Characterisation of the central nervous depressant activity of a commercially available valerian root extract. Arzneimittelforschung 1993;43:638-41
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20. Krieglstein J, Grusla D. Centrally depressant components of valerian. However, valepotriates, valerenic acid, valeranone and the essential oil are ineffective [in German]. Dtsch Apoth Ztg 1988;128:2041-6 21. European Scientific Cooperative on Phytotherapy. Valerianae radix. Exeter, UK: ESCOP 1996-1997:3-4 Monographs on the Medicinal uses of Plant Drugs, Fascicule 4 22. Resecrans JA, Defeo JJ, youngken HW Jr. Pharmacological investigation of certain Valeriana officinalis L. extracts. J Pharm Sci 1961l50:240-4 23. Willey LB, Mady SP, Cobaugh DJ, et al. Valerian overdose: a case report. Vet Hum Toxicol 1995;37:364-5 24. Chan TY, Tang CH, Critchley JA. Poisoning due to an over-the-counter hypnotic, Sleep-Qik (hyoscine, cyproheptadine, valerian). Postgrad Med J 1995;71(834):227-8 25. Chan TY. An assessment of the delayed effects associated with valerian overdose [letter]. Int J Clin Pharmacol Ther 1998;36:569 26. Hendriks H, et al. Central nervous depressant activity of valerenic acid in the mouse. Planta Med Feb1985;1:28-31 27. Houghton PJ. The biological activity of valerian and related plants. J Ethnopharmacol 1988;22(2):121-42 28. Santos MS, et al. Synaptosomal GABA release as influenced by valerian root extract involvment of the GABA carrier. Arch Int Pharmacodyn Ther 1994;327(2):220-31 29. Houghton PJ. The scientific basis for the reputed activity of valerian. J Pharm Pharmacol May 1999;51(5):505-12 30. Houghton PJ. The biological activity of valerian and related plants. J Ethnopharmacol 1988;22(2):121-42 31. Santos MS, et al. Synaptosomal GABA release as influenced by valerian root extract involvment of the GABA carrier. Arch Int Pharmacodyn Ther 1994;327(2):220-31 32. Houghton PJ. The scientific basis for the reputed activity of valerian. J Pharm Pharmacol May1999;51(5):505-12 33. Houghton PJ. The biological activity of valerian and related plants. J Ethnopharmacol 1988;22(2):121-42 34. Santos MS, et al. Synaoptosomal GABA release as influenced by valerian root extract involvment of the GABA carrier. Arch Int Pharmacodyn Ther 1994;327(2):220-31 35. Houghton PJ. The scientific basis for the reputed activity of valerian. J Pharm Pharmacol May1999;51(5):505-12
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Vinpocetine
General Features
Vinpocetine is a derivative of the Vinca minor (lesser periwinkle), which is native to many parts of Europe, where it grows in woods and thickets. The isolated active constituent known as ethyl apovincaminate was discovered in the late 1960s and since that time has been studied and used as a natural agent to enhance blood flow to the brain, with particularly emphasis on its potential use in cerebral vascular insufficiency, dementia and ischaemic stroke.1,
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superior to placebo in ratings of the severity of illness. There were no serious side effects reported from the use of Vinpocetine and adverse events between Vinpocetine-treated patients and the placebo group were comparable, indicating no increased attributable risk from the use of Vinpocetine. 6 In regards to Alzheimers disease, experimental evidence has shown that Vinpocetine protects brain cells from the toxic effects of Amyloid beta-Protein (Abeta-Protein), which is the agent known to damage brain cells in the development of Alzheimers disease. Abeta-Protein induces free radical damage, which in turn, leads to severe damage to the energy factories (mitochondria ) of the cell, vital enzymes (especially those needed to produce the memory chemical, acetylcholine) and other cellular structures. Uncontrolled free radical damage of this nature can ultimately lead to brain cell death of affected neurons. Vinpocetine has been shown to quench (neutralize) free radicals produced by Abeta-Protein, reducing the oxidative damage (free radical) to brain cells under experimental conditions. It also has been shown to protect key respiratory chain complexes within the mitochondria (energy factories of the cell) that were exposed to Abeta-Protein. The researchers conclude that Vinpocetine can exert neuroprotective properties which might be of importance and contribute to its clinical efficacy in the treatment of Alzheimers disease or other neurodegenerative disorders in which oxidative stress is involved (e.g., Parkinsons disease, Multiple sclerosis etc.) 7 As reviewed by CD Nicholson, Vinpocetine attenuates cognitive deficits, reduces ischaemia-induced hippocampal cell loss and increases cerebral blood flow and glucose utilization. 8 Many scientists indicate that Vinpocetines ability to improve cognitive function is primarily due to its effects on enhancing blood flow to the brain, dilating blood vessels, supporting the proper function of red blood cells and reducing blood viscosity via its influence on reducing platelet stickiness.9,10,11
Drug-Nutrient Interactions
Anti-Coagulant Medications (e.g., Aspirin, Coumadin, Warfarin): Vinpocetine may potentiate the effects of these drugs increasing the risk of a bleeding disorder in the brain or elsewhere in the body. Thus, it is contraindicated in these cases, as is Ginkgo Biloba, which affects the brain in a similar fashion as Vinpocetine.4
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1.
Bnczk P, Gulys B, Adam-Vizi V, Nemes A, Krpti E, Kiss B, et al. Role of sodium channel inhibition in neuroprotection: effect of vinpocetine. Brain Res Bull Oct2000;53(3):p245-54 2. Dietary Supplement Information Bureau: Vinpocetine. www.content.intramedicine.com. Dietary Supplement Education Alliance 2001 3. Feigin VL, Doronin BM, Popova TF, Gribatcheva EV, Tchervov DV. Vinpocetine treatment in acute ischaemic stroke: a pilot single-blind randomized clinical trial. Eur J Neurol Jan2001;8(1):p81-5 4. Kidd PM. A review of nutrients and botanicals in the integrative management of cognitive dysfunction. Alternative Medicine Review (ALTERN MED REV) Jun1999;4(3):144-61 5. Balestreri R, Fontana L, Astengo F. A double-blind placebo controlled evaluation of the safety and efficacy of Vinpocetine in the treatment of patients with chronic vascular senile cerebral dysfunction. J Am Geriatr Soc 1987;35:425-30 6. Hindmarch I, et al. Efficacy and tolerance of vinpocetine in ambulant patients suffering from mild to moderate organic psychosyndromes. Int Clin Psychopharmacol 1991;6(1):31-43 7. Pereira C, Agostinho P, Oliveira CR. Vinpocetine attenuates the metabolic dysfunction induced by amyloid beta-peptides in PC12 cells. Free Radic Res Nov2000;33(5):p497-506 8. Nicholson CD. Pharmacology of nootropics and metabolically active compounds in relation to their use in dementia. Psychopharmacology (Berl) 1990;101:147-59 9. Burtsev EM, et al. [10-year experience with using Cavinton in cerebrovascular disorders]. Zh Nevropatol Psikhiatr Im S S Korsakova 1992;92(1):56-60 10. Tamaki N, et al. The effect of Vinpocetine on cerebral blood flow in patients with cerebrovascular disorders. Ther Hung 1985;33:13-21 11. Osawa M, Maruyama S. Effects of TCV-3B (Vinpocetine) on blood viscosity in ischemic cerebrovascular disease. Ther Hung 1985;33:712
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Osteoarthritis: A double-blind placebo-controlled trial of 78 subjects with osteoarthritis of the knee or hip also showed that white willow extract was effective in decreasing pain and improving joint function compared to the placebo.1 2. Headache Some evidence suggests that White Willow Bark extract may be helpful in the treatment of certain headaches. 7,8,17
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Drug-Nutrient Interactions
White Willow Bark extract may interact with other drugs in a similar fashion as ASA, producing a negative health effect. Although no reports of White Willow Bark extract have been reported practitioners should be alerted to the following potential drug-nutrient interactions with salicin: Drug Acebutoiol Adrenocorticoids (systemic) Alendronate (biphosphanate) Allopurinol ACE Inhibitor Antacids Anticoagulants Anti-diabetic agents (oral) Anti-inflammatory drugs (NSAIDs) Bumetanide Carteolol Combined Effect Decreased anti-hypertensive effect of acebutoiol Increased adrenocorticoid effect Increased risk of stomach irritation if taken within 30 minutes of Alendronate Decreased allopurinol effect by increasing kidney resorption of uric acid Decreased ACE inhibitor effect (angiotensinconverting enzyme) anti-hypertensive drugs Decreased aspirin effect Increased anti-coagulant effect (abnormal bleeding) Low blood sugar Risk of stomach, intestinal bleeding and ulcers Possible aspirin toxicity Decreased anti-hypertensive effect of carteolol 3,1
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Bradley PR, et.al., British Herbal Compendium, Vol.1, Bournemouth, Dorset, UK, British Herbal Medicine Association 1992, 224-226 Meier B, et.al., Pharmaceutical Aspects of the Use of Willows in Herbal Remedies, Planta Medica, 54, 1988, 559-560. Newall C, Anderson L, Phillipson J, Herbal Medicines. A Guide for Health Care Professionals, London: The Pharmaceutical Press, 1996, 296. Meier B, et.al., Identifikation und Bestimmung Von Je Acht Phenolglykosiden in Salix Purpurea und Salix Daphnoides Mit Moderner HPLC, Pharmaceutica Acta Helvetica 60, 1985, 269-274. Mills SY, et.al., Effect of a Proprietary Herbal Medicine on the Relief of Chronic Arthritic Pain: A Double-blind Study, Br J Rheum, 35, 1996, 874-878. Tyler V, Herbs of Choice. The Therapeutic Use of Phytomedicinals, Binghampton: Pharmaceutical Products Press, 1994, 209. ESCOP, Salicis Cortex/Willow Bark, In: ESCOP Monograph Fascicule 4 Exeter, ESCOP, 58, 1997. Hoffmann D, Holistic Herbal, Rockport, CA: Element Books, 1996, 256. Blumenthal M, et.al., The Complete Commission E Monographs: Therapeutic Guide to Herbal Medicines, Boston, MA: Integrative Medicine Communications, 1998, 230. Griffith HW, Complete Guide to Non Prescription and Prescription Drugs, The Body Press / Perigee, 1998, 132-133. Natural Products Encylopedia. http://www.consumerslab.com/: White Willow Krivoy N, Pavlotsky E, Chrubasik S et al. Effect of Salicic cortex extract on human platelet aggregation. Planta med 2000;66:1-4 European Scientific Cooperative on Phytotherapy. Salicis cortex. Exeter UK: ESCOP; 1996-1997:p2. Monographs on the medicinal uses of plant drugs, fascicule 4. Foster S. 1010 Medicinal Herbs. Interweave Press, Loveland CO 1998:210-1 Healthnotes Inc. 2001. www.healthnotes.com: Willow Chrubasik S, Eisenberg E, Balan E et al. Treatment of low back pain exacerbations with willow bark extract: a randomized doubleblind study. Am J Med 2000;109:9-14 Schmid B, Ludtke R, Selbmann HK et al. Efficacy and tolerability of a standardized willow bark extract in patients with osteoarthritis: randomized, placebo-controlled, double blind clinical trial [translated from German.] Z Rheumatol 2000;59:314-20 Weiss RF. Herbal Medicine. Ab Arcanum, Gothenburg, Sweden 1988;31:p303
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Drug-Nutrient Interactions
No well-known drug-nutrient interactions exist for Wild yam at this time.2,7
1. 2. 3. 4. 5. 6. 7. 8.
Hudson T. Wild yam, natural progesterone, unraveling the confusion. Townsend Letter for Doctors and Patients 1996;July:1257 Boon H, Smith M.The Botanical Pharmacy. Quarry health Books 2000:314-6 Araghiniknam M, Chung S, Nelson-White T, Eskelson C, Watson RR. Antioxidant activity of dioscorea and dehydroepian drosterone (DHEA) in older humans. Life Sciences 1996;59(11):147-57 Dollbaum C. Lab analyses of salivary DHEA and progesterone following ingestion of jaym-containing products. Townsend Newsletter for Doctors 1996;159:104 Chevalier A. The Encyclopedia of medicinal Plants. London: Readers Digest 1996:336 Hoffmann D. holistic Herbal. Rockport, CA: Element Books 1996:256 Healthnotes Online. Healthnotes, Inc 2000 Craddick J. Potential hazards of Mexican yam. Townsend Letter for Doctors and Patients 1996Aug/Sept:101
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