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Chaparral

Chaparral

Botanical Description & Habitat

Larrea divaricata

Family
Zygophyllaceae

Common Names
Chaparro
Creosote bush
Dwarf evergreen oak
Grease wood
Gobonadora
Hediondilla

Habitat
Southwestern United States and northern Mexico; dry desert areas.

Description
Chaparral is a perennial plant growing from 2-9 feet in height. The stem is dark green and erect; the leaves are strong-scented and resinous, consisting of 2 small leaflets. Small, bright yellow, 5-petal flowers bloom in spring and winter. The fruit is a small globose seed capsule, covered with white hairs.

Medicinal Parts
Leaves and stems

Historical Properties & Uses

In Native American folklore and in modern science, chaparral has a variety of positive qualities. Indeed, it is referred to as the "penicillin of hydroquinones."

Chaparral is used mainly to treat cancer, arthritis, and rheumatism. Its primary active component, nordihydroquaiaretic acid (NDGA), possesses analgesic and circulatory depressant properties. On the cellular level, NDGA exhibits several effects accounting for its efficacy in treating cancer and arthritis: it increases ascorbic acid levels in the adrenals, and it is antioxidant and anti-cancerous in action.

Chaparral gained notoriety in the 1970's with the publication of sensational clinical trials indicating chaparral tea could positively affect the course of skin cancer. Although those trials apparently inspired no further research in that area, animal studies have indicated NDGA almost completely inhibits both aerobic and anaerobic glycolysis and respiration in some kinds of cancer cells.

Method of Action

This is one case in which the amount of research on an herb seems to be larger than the body of folklore surrounding it.

The primary active constituent of chaparral is nordihydroguaiaretic acid (mercifully shortened to NDGA), which has received much research attention because it is a powerful antioxidant, and has shown much potential for use in the food processing and pharmaceutical industries.

NDGA possesses analgesic and vasodepressant action. Chaparral increases the ascorbic acid levels of the adrenal glands, thereby helping to reduce inflammation. Chaparral has confirmed antioxidant and anticancer properties. On a cellular level NDGA stimulates mitochondrial respiration.

NDGA, due to its antioxidant nature, significantly inhibits the formation of dental caries. The antibacterial nature of NDGA and of chaparral has been substantiated in other studies. For example, it is effective against staphylococcus aureus, s. albus, salmonella typhi, s. typhimurmium, and various proteus strains.

Some research has demonstrated on analgesic action in NDGA. It helps to reduce the painful symptoms of rheumatism.

NDGA may even help retard aging. Feeding this anti-oxidant in the amount of 20 mg/kg to rats significantly increased the life span of males and females and increased the number of litters born by the females during their lifetime, as compared to controls.

Regarding cancer, NDGA produces almost complete inhibition of aerobic and anaerobic glycolysis and respiration in some kinds of cancer cells without affecting normal cells.

The disruption of cellular enzymatic pathways plays an important role in the etiology of cancer. The faulty metabolism of arachidonic acid and other unsaturated fatty acids may produce carcinogenic by-products. It has been repeatedly shown NDGA (technically classified as a lipoxygenase inhibitor) prevents the formation of cancerous cells by the above route. This line of research promises to validate the use of chaparral and elucidate the mechanism by which it prevents and/or cures cancer.

In the late 1960's, a report appeared concerning a man who had cured his skin cancer by consuming huge quantities of chaparral tea. The case was remarkable because standard forms of therapy had utterly failed. The same year, a follow-up study on the use of two to three glasses of chaparral tea per day, or 250-3,000 mg of pure NDGA per day to treat 59 cases of "incurable" cancer found while some patients improved, most stayed the same or got worse.

The authors concluded chaparral is not an effective cancer treatment. However, the study did not indicate which patients received which treatment, nor which received high or low doses, nor which improved and which didn't, nor even how long each patient was treated.

Much more work is needed in the application of chaparral or NDGA in the treatment of cancer (hopefully not always of the incurable kind) before we will know when it will work, for whom it will work, how much is required, or how long treatment should be given.

Drug Interactions & Precautions

Possible Interactions
The anti-inflammatory activity of chaparral can be seriously inhibited by phenobarbital as well as by certain other sedatives and hypnotics, such as chloral hydrate and meprobamate. This is also true of beta-adrenergic blocking agents, such as propranolol.

Comments
The presence of azulenes in chaparral may interfere with actions of bradykinin, histamine, acetylcholine, and serotonin.

There is evidence combined use of bactericidal and bacteriostatic agents will lower the effectiveness of the bacteriostatic agent. However, how this finding applies to herbal anti-infectives is still unknown.

Safety Factors & Toxicity

The FDA currently considers Chaparral to be a toxic substance.

All victims took chaparral tablets or capsules for between 6 weeks and 3 months.

The toxicity of chaparral itself appears to be very low. Contrary to some reports, chaparral does not contain any creosote. It is often called the creosote bush because of its creosote-like smell.

NDGA fed to rats at levels of 0.5 and 1.0% in the diet for 74 weeks caused cystic reticuloendotheliosis of paraceaecal lymph nodes and vacuolation of kidney tubular epithelium. This dose is several orders of magnitude greater than normal human consumption.

NDGA at levels of 0.5% in the diet for two year periods has caused inflammatory caecal lesions and slight cystic enlargement of paracaecal lymph nodes. Growth inhibition occurred after the first 6 months at levels of ).5 and 1.0%. In another experiment, 0.5% caused massive caecal hemorrhages with single or multiple mesenteric cysts.

But others have found 0.5% NDGA in the diet had no marked effect on food intake, nor on kidneys, liver and spleen.

Preparation & Administration

Three times a day

Tea
tea made from 1/2 tsp dried herb

Purified nordihydroguaiaretic acid
250 mg

Note: This Herbal Preparation information is a summary of data from books and articles by various authors. It is not intended to replace the advice or attention of health care professionals.

References

Am Hospital Formulary Service. Am Soc of Hosp Pharm. Wash, D.C.

Bergel, M. Empleo del acido nordihydroquayaretico en thereutica. Semana Medical, (Buenos Aires), 11, 123, 131, 1955.

Bressler, R., M.D. Bogdonoff & G.J. Subak-Sharpe. 1981. The Physicians Drug Manual. Doubleday & Co, Inc. Garden City, NY. 1213 pp.

Burk, D. & M. Woods. Hydrogen peroxide catalase, glutathion peroxidase, quinones, nordihydroquaiaretic acid, and phophopyridine nucleotides in relation to x-ray action on cancer cells. Radiation Research Supplement, 3, 212-246, 1963.

Buu-Hoi, N.P. & A.R. Ratsimamanga. Action retardante de l'acide nordihydroguaiaretique sure le vieillissement chez le rat. Comptes Rendus des Seances de la Societe de Biologie et de ses Filiales, 153, 1180-1182, 1959.

Carine, K. & D. Hudig. Assessment of a role for phospholipase A2 and arachidonic acid metabolism in human lymphocyte natural cytotoxicity. Cellular Immunology, 87(1), 270-283, 1984.

Clark, T., A. Conney & B. Harpole, et.al. 1967. Drug interactions that can affect your patients. Patient Care, 1(11). pp. 33-71.

Cranston, E.M., et. al. The acute and chronic toxicity of nordihydroquaiaretic acid. Federation Proceedings, Federation of American Society of Experimental Biology, 6, 318, 1947.

Epstein, S.S., I.B. Sporoschetz & S.H. Hunter. Toxicity of antioxidants to tetrahymena pyriformis. Journal of Protozoology, 14(2), 238-244, 1967.

Facts and Comparison. The Lawrence Review of Natural Products. Aug, 1993.

Felter, H.W. & J.U. Lloyd. King's American Dispensatory, 18th Ed. 1898. reprinted by Eclectic Medical Publications: Portland, OR, 1983.

Goodman, L.S. & A. Gilman. 1975. Pharm Basis of Thera. MacMillan, NY.

Grice, H.C., G. Becking & T. Goodman. Toxic properties of nordihydroguaiaretic acid. Food and Cosmetics Toxicology, 6, 155-161, 1968.

Hansten, P.D. 1979. Drug Interactions, 4th ed. Lea & Febiger, Phila.

Herrman, K. Lignans and their practical importance. Pharmazie, 12, 147-155, 1957.

Hirose, K., Y. Ose & J. Kitamura. Antbacterial property of antioxidants. Gifu Yakka Daigaku Kiyo, 6, 66, 1956.

Kastrup, E.K., ed. 1981. Drug Facts and Comparisons, 1982 edition. Facts and Comparisions Division, J.P. Lippincott Co, Phila(St. Louis).

Katz, M et al., Herbal hepatitis: subacute hepatic necrosis secondary to chaparral leaf. J. Clin. Gastroenterol. 1990, 12:203.

Jelicic-Hadzovic, J. & P. Stern. 1972. Azulenes and bradykinins. Arzneimittel-forschungen, 22(7). pp. 1210-1211.

Lehman, A.J., et. al. The pharmacological evaluation of antioxidantes. Adv. Fed. Res., 3, 197- 1951.

Lewis, Walter H. and Elvin-Lewis, Memory P.F. Medical Botany: Plants Affecting Man's Health, John Wiley and Sons. New York, l977.

Lisanti, V.F. & B. Eichel. Antioxidant inhibition of experimentally induced caries. Journal of Dental Research, 42, 1030-1035, 1963.

List, P. & L. Hoerhammer. 1969-1976. Hagers Hanbuch der Pharmazeutischen Praxis, vols. 2-5. Springer-Verlag, Berlin.

Martin, E. Drug Interactions Index, 1978/79. J.B. Lippincott Co., Phila.

MMWR Chaparral-induced toxic hepatitis. California and Texas, 1992. MMWR. 1992, 43:812.

Mowrey, Daniel B., Ph.D. Exper. Psych., Brigham Young University. Director of Nebo Institute of Herbal Sciences. Director of Behavior Change Agent Training Institute. Director of Research, Nova Corp.

Riesterer & Jaques. 1968. Interference by beta-adrenergic blocking agents with the antiinflammatory action of various drugs. Helv Physiol Acta, 26. pp. 287-293.

Schaffler and Reeh : Double-Blind Study of the Hypoxia-protective Effect of a Standardized Ginkgo Biloba Preparation After Repeated Administration in Healthy Volunteers. Arzneim-Forsch 35:1283- 6, 1985.

Schwarz, Peres, Kunz., et. al. On the role of superoxide anion radicals in skin tumor promotion. Carcinogenesis, 5(12), 1663-1670, 1984.

Smart, C.R., et. al. An interesting observation on nordihydroquaiaretic acid (nsc-4291; NDGA) and a patient with malignant melanoma--a preliminary report. Cancer Chemotherapy Reports, Part 1, 5392), 147-151, 1969.

Smart, C.R., et. al. Clinical experience with nordihydroquaiaretic acid-chaparrel (sic) tea in the treatment of cancer. Rocky Mountain Medical Journal, November, 1970, 39- 43.

Sporn, A. & O. Schobesch. Cercetari cu privire la toxicitatea acidului nordihidrogaiaretic (NDGA). Igiena, (Bucharest), 15(12), 725-726, 1966.

Stuart, D.M. 1968. Drug metabolism Part 2. Drug interactions. PharmIndex, 10(10). pp. 4-16.

Valone, F.H., et. al. Enhanced arachidonic acid lipoxygenation by K562 cells stimulated with 12-0-tetradeconolylphorbo-13-acetate. Cancer Research, 43(1), 197-201, 1983.

Waller, C.W. & O.N. Gisvold. A phytochemical investigation of larrea divaricata cav. Journal of the American Pharmaceutical Association, 34, 78-81, 1945.

 


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