Botanical Description & Habitat
Cleaver grass Cow grass Honey suckle clover Marlgrass Meadow clover Purple clover Wild clover
Common throughout North America, Europe, and central and northern Asia. It flourishes in fields, meadows, and along roadsides.
Has an erect, branching, reddish stem, one to two feet in height, with white hairs. The leaves are composed of three oval leaflets which are toothed and grow on alternate sides of the stem. Flowers range from white to purple, and grow in dense clusters, forming an ovoid flower head.
Flowering tops, fresh or dried, gathered just after flowering.
Historical Properties & Uses
Several properties of red clover are recognized in Eastern as well as Western cultures. Both groups use red clover as an important rejuvenator, a diuretic in gout, a sedative in bronchial conditions, and an antitussive in whooping cough. It is used by both cultures to treat debilitating, infectious, and inflammatory diseases, ie. asthma, bronchitis, ulcers, skin ailments, rheumatism, arthritis. Red clover has long been used as a cancer treatment by many cultures. The most modest claims admit the herb will not cure malignancies, but may prevent them from returning once removed.
Many Western herbalists believe it acts primarily as a potent alterative. Although a chemical basis for this claim has not been found, several individual properties have been substantiated that together may add up to an alterative effect.
Method of Action
Red clover has moderate anti-inflammatory activity
In anti-inflammatory screening tests on the activity of plants against carrageenin-induced rat pedal edema tests, red clover exhibited moderate activity (43% inhibition).
Red clover has some antitubercular and bacteriostatic action
Incubated at 37 degrees C. for seven days with the H37Rv strain of Mycobacterium tuberculosis, red clover extract produced inhibition at concentrations lower than 1:80 but higher than 1:40, only moderately active. A tea made from red clover tops was shown to inhibit the growth of unspecified bacteria.
Red clover is estrogenic
In the 40 years following the introduction of subterranean clover to Australia, disturbances in fertility become widespread among grazing animals. Eventually, the cause was attributed to isoflavones in the leaf. Once the structure of these isoflavones was determined, it was noticed they strongly resembled certain steroids. While searching for the cause of fertility problems, researchers noticed this clover, when grown in phosphate-poor soil, produced an enormous rise in estrogenic effects (rise in uterus weight of test animals by 15-20%). This led some investigators to the conclusion fertility problems were based on a rise in the concentration of isoflavones as a result of insufficient phosphate- (possibly sulphate-) rich fertilizer.
Based upon these observations and studies, European investigators began to test their native red clover. Red clover contains 4 to 7 times less isoflavone concentration as the Australian variety. The isoflavones of red clover are weaker in action than the other species (biochanin A & formononetin versus, and only traces of genistein, the strongly active flavone found abundantly in subterranean clover). Red clover was found to possess only small estrogenic activity. Increasing phosphate deficiency and increasing general manure treatment increased the isoflavone concentration. Although not enough to cause significant estrogenic effects on animals. Red clover, therefore, possesses no estrogenic threat to animals, but does possess mild estrogenic activity. The estrogenic property is due to whatever genistein and/or coumarin content is present, some varieties being more potent than others.
Red clover's antispasmodic and expectorant properties are recognized in the Merck Index.
Is red clover an anti-cancer agent?
This question has not been adequately addressed in research literature. Considering the number of cultures using it for that purpose and the length of time it has been so used, the question requires solution.
Drug Interactions & Precautions
The presence of estrogen-like substances in red clover may increase the production of procoagulant factors which, in turn, may inhibit the anticoagulant action of heparin or coumarin. The estrogenic constituents of this plant may also potentiate oral antidiabetics, folic acid antagonists, and some corticosteroids.
Conversely, the presence of estrogen in this herb can inhibit antihypercholesterolemics by inducing hyperlipemia. It can also inhibit the activity of most parenteral medications by reducing the rate of spreading. However, the estrogenic activity of red clover may be inhibited by meprobamate and phenobarbital.
Due to the presence of estrogenic substance, oxytocin may augment the neural conductivity and contractility of uterine smooth muscle. The estrogen in this herb may also raise blood glucose levels enough to alter insulin requirements in diabetics.
The antituberculous activity of red clover may potentiate the adverse effects of other antituberculous drugs, especially ethionamide.
Conversely, the antiarrhythmic agent, quinidine, may increase the hypoprothrombinemic effect of this herb.
Allopurinol has been tentatively shown to increase the half-life of anticoagulants.
Although the coumarin content of red clover is low at normal usage levels, it is important to note coumarins can affect the action of almost any drug.
Safety Factors & Toxicity
Red clover causes trifoliosis, a dermatitis due to photosensitization in animals. Human toxicity is rare.
Preparation & Administration
Three times a day
made from 1 tsp of dried flower
1:1 in 25% alcohol, 1.5-3 ml
1:10 in 45% alcohol, 1-2 ml
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.
Albert-Puleo, M. 1980. Fennel and anise as estrogenic agents. Journal of Ethnopharmacology, 2. pp. 337-344.
Alexander, G. & Rossiter, R.C: Aust J Of Agr Res, 3, 24-28, 1952.
Am Hospital Formulary Service. Am Soc of Hosp Pharm. Wash, D.C.
Bennetts, H.W., Underwood, E.J. & Shier, F.L. Australian Veternary Journal, 22, 2-12, 1946.
Bressler, R., M.D. Bogdonoff & G.J. Subak-Sharpe. 1981. The Physicians Drug Manual. Doubleday & Co, Inc. Garden City, NY. 1213 pp.
Ch'ang, T.S Nature (London), 182, 1175, 1958.
Clark, T.H., A.H. Conney & B.P. Harpole, et.al. 1967. Drug interactions that can affect your patients. Patient Care, 1(11). pp. 33-71.
Committee on Pharmocopaeia of the Am Institute of Homeopathy, The Homeopathic Pharmacopaeia of the United States. 8th ed., Vol 1. Otis Clapp and Son, Agents, Boston, l981.
Costello, C.H. & C.L. Butler. 1950. The estrogenic and uterine-stimulating activity of asclepias tuberosa. A preliminary investigation. J of the Am Pharm Assoc, 39. pp. 233-237.
Curnow, D.H. Biochem. Journal, 58, 283-287, 1954.
Drug package insert (FDA approved official brochure) and other labeling based on sponsored clinical investigations and New Drug Application data.
Fitzpatrick, F.K. Plant substances active against mycobacterium tuberculosis. Antibiotics And Chemotherapy, 4(5), 528-536, 1954.
Goodman, L.S. & A. Gilman. 1975. Pharm Basis of Thera. MacMillan, NY. Hansten, P.D. 1979. Drug Interactions, 4th ed. Lea & Febiger, Phila.
Goodman, L. & A. Gilman. 1975. The Pharmacological Basis of Therapeutics. MacMillan, New York.
Hansten, P.D. 1975. Personal observations of patients. Drug Interactions. 3rd ed. Lea & Febiger, Philadelphia. pp. 25, 213.
Hyde, F.F. British Herbal Pharmacopoeia. British Herbal Medicine Assoc: West Yorks, England, 1983
Kastrup, E.K., ed. 1981. Drug Facts and Comparisons, 1982 edition. Facts and Comparisions Division, J.P. Lippincott Co, Phila(St. Louis).
Koch-Weser, J. 1968. Quinidine-induced hypoprothrombinemic hemorrhage in patients on chronic warfarin therapy. Annals of Internal Medicine. 68(3). pp. 511-517.
Krause, E. Acta Vet.(brno), 39, 279, 1970; Through Chem Abstracts, 74, 85885T, 1971.
Legg, S.P., et. al., Biochemistry Journal, 46, xix, 1950.
Link, K: The discovery of dicumarol and its sequels. Circulation, 1959, 19:97-107.
List, P. & L. Hoerhammer. 1969-1976. Hagers Hanbuch der Pharmazeutischen Praxis, vols. 2-5. Springer-Verlag, Berlin.
Martin, E.W. 1978. Drug Interactions Index, 1978/79. J.B. Lippincott Company, Philadelphia.
Merck. The Merck Index: An Encyclopedia Of Chemicals And Drugs. 9th edition, Rahway, N.J.: Merck & Co., 1976.
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.
Nelson, D.H., et.al. 1963. Potentiation of the biologic effect of administered cortisol by estrogen treatment. Journal of Clin Endocrinology and Metabolism, 23(3). pp. 261-265.
Newall CA, Anderson LA, Phillipson JD. Herbal Medicines A Guide for Health-care Professionals. London: The Pharmaceutical Press, 1996:21,45,63,282.
Rolinski, Z. Ann. Univ. Mariae Curie-sklodowska, Sect D D, 24, 187, 1970. Through Chem Abstr., 75, 150167X, 1971.
Schultz, G. Ueber den gehalt an oestrogenwirksamen isoflavonen in rotklee (trifolium pratense L.) nach anzucht in wasser-sand-kultur mit unterschiedlicher mineralsalzversorgung. Deutsche Tieraerztliche Wochenschrift, 74(5), 118-120. 1967.
Scientific Committee, British Herbal Pharmocopaeia, British Herbal Med Assoc, Lane House, Cowling, Na Keighley, West Yorks, Bd Bd220lx, l983
Spangler, A.S., et.al. 1969. Enhancement of the antiinflammatory action of hydrocortisone by esrtogen. J of Clin Endoc, 29(5). p.650-655.
Stuart, D.M. 1968. Drug metabolism Part 2. Drug interactions. PharmIndex, 10(10). pp. 4-16.
Tuskaev, A.K. Rast. Resur., 7, 295, 1971; Through Chem Abstacts 75, 85222V, 1971.
Udall, J.A. 1968. Quinidine and hypoprothrombinemia. Annals of Internal Medicine, 69(8). pp. 403-404.
Vessell, E.S., et.al. 1970. Impairment of drug metabolism in man by allopurinol and nortriptyline. New England J of Med, 283. p. 1484.
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