Latin name; Tanacetum parthenium

Other names: Feverfew, featherfew, altamisa, bachelor’s button, featherfoil, febrifuge plant,

About Feverfew

Feverfew (Tanacetum parthenium L.) belongs to the family Asteraceae (daisies). It is a daisy-like perennial plant found commonly in gardens and along roadsides. The name stems from the Latin word febrifugia, “fever reducer.” The first-century Greek physician Dioscorides prescribed feverfew for “all hot inflammations.” Also known as “featherfew,” because of its feathery leaves (1-3). Native to the Balkan Peninsula, feverfew is now found in Australia, Europe, China, Japan, and North Africa. In the mid-19th century, feverfew was introduced in the United States. The plant grows along roadsides, fields, waste areas, and along the borders of woods from eastern Canada to Maryland and westward to Missouri.

The plant has been used to treat arthritis, asthma, constipation, dermatitis, earache, fever, headache, inflammatory conditions, insect bites, labour, menstrual disorders, potential miscarriage, psoriasis, spasms, stomach ache, swelling, tinnitus, toothache, vertigo, and worms. Feverfew also has been used as an abortifacient, as an insecticide, and for treating coughs and colds. Traditionally, the herb has been used as an antipyretic, from which its common name is derived. (4-9).

The leaves are ingested fresh or dried, with a typical daily dose of 2–3 leaves. The bitterness is often sweetened before ingestion. Feverfew also has been planted around houses to purify the air because of its strong, lasting odour, and a tincture of its blossoms is used as an insect repellant and balm for bites (2).

The most important biologically active principles are the sesquiterpene lactones, the principal one being parthenolide. Parthenolide is found in the superficial leaf glands (0.2%–0.5%), but not in the stems, and comprises up to 85% of the total sesquiterpene content (4,6,10).It also contains flavonoids and volatile oils

Uses of Feverfew


A great deal of interest has focused on the activity of feverfew in the treatment and prevention of migraine headaches (11).

A study in 8 feverfew-treated patients and 9 placebo-control patients found that fewer headaches were reported by patients taking feverfew for up to 6 months of treatment. Patients in both groups self-medicated with feverfew for several years before enrolling in the study. The incidence of headaches remained constant in those patients taking feverfew but increased almost 3-fold in patients who switched to placebo during the trial (12). The abrupt discontinuation of feverfew caused incapacitating headaches in some patients. Nausea and vomiting were reduced in patients taking feverfew, but the statistical analysis has been questioned (13). These results were confirmed in a more recent placebo-controlled study in 72 patients suffering from migraine (14). On the basis of their research, investigators predicted that feverfew may be useful not only for classical migraine and cluster headaches, but also for premenstrual, menstrual, and other headaches (15).

However, studies at the London Migraine Clinic found that the experimental observations may not be clinically relevant to migraine patients taking feverfew (16). The clinical efficacy and safety of 3 dosage regimens of a carbon dioxide (CO2) feverfew extract, each given 3 times daily, were compared with placebo in a double-blind, multicentre, randomized, controlled trial. One hundred forty-seven patients suffering from migraine with or without aura according to International Headache Society criteria were treated. The primary end point was the total number of migraine attacks during the last 28 days of treatment compared with the 4-week baseline period. Secondary end points were total and average duration, intensity of migraine attacks, and number of days with accompanying migraine symptoms. There were no statistically significant effects for primary or secondary end points. Furthermore, a dose–response relationship was not observed.
Subgroup analysis of 49 patients with at least 4 migraine attacks during the baseline period showed a significant effect with the 6.25 mg dose compared with placebo (P = 0.02) (17).

A Cochrane review of evidence from double-blind, randomized, controlled trials was inconclusive in establishing the efficacy of feverfew for preventing migraine headaches. Results from the meta-analysis reported insufficient evidence to conclude whether feverfew was superior to placebo in reducing the frequency and severity of migraine attacks, incidence and severity of nausea and vomiting, and global assessment of efficacy in patients with migraine headaches. The dosage form varied in the trials, and thus may have impacted the results (9,18).
Three trials administered dried powdered feverfew leaf extract at 50-100 mg/day for 8–24 weeks; 1 trial administered an alcoholic feverfew extract 143 mg/day for 8 weeks; 1 trial administered a CO2 extract (2.08 mg vs 6.25 mg vs 18.75 mg 3 times daily for 12 weeks). The 2 studies with the highest methodologic quality administered the alcoholic and CO2 extract and reported no benefit, whereas the studies with lower methodologic quality administered the dried powdered leaf extract reported a favorable response (9).

Feverfew may produce an antimigraine effect in a manner similar to methysergide maleate (Sansert), a known 5-HT antagonist (19,20).

Anti-inflammatory effects

Extracts of the plant also inhibit the release of enzymes from white cells found in inflamed joints, and a similar anti-inflammatory effect may occur in the skin, providing a rationale for the traditional use of feverfew in psoriasis.

Rheumatoid arthritis

The effect of feverfew on rheumatoid arthritis has been investigated in a double-blind, randomized, placebo-controlled trial. Forty-one women with rheumatoid arthritis were randomized to take placebo or feverfew 70–86 mg for 6 weeks. Of the 15 parameters tested, only grip strength improved significantly (P = 0.04) in the feverfew group compared with the placebo group. Human synovial fibroblasts express an intracellular adhesion molecule-1 (ICAM-1) that has been implicated in the pathogenesis of rheumatoid arthritis. Feverfew extracts or purified parthenolide inhibited the increased expression of ICAM-1 on human synovial fibroblasts by cytokines IL-1, TNF-α, and interferon-γ (7,21,22).


Feverfew may alter the effects of some prescription and non-prescription medications (23). Feverfew may inhibit the activity of platelets, so individuals taking anticoagulants (such as aspirin and warfarin) should consult a health care provider before taking this herb (19).

Patients who switched to placebo after taking feverfew for several years experienced a cluster of nervous system reactions (eg, headaches, insomnia, joint pain, nervousness, poor sleep patterns, stiffness, tension, tiredness) along with muscle and joint stiffness, often referred to as “postfeverfew” syndrome (12, 23). In a larger series of feverfew users, 18% reported adverse effects, the most serious being mouth ulceration (11%). Feverfew can induce more widespread inflammation of the oral mucosa and tongue, often with lip swelling and loss of taste. Dermatitis has been associated with this plant (11, 24).

Pregnant women should not use the plant because the leaves have been shown to possess potential menstruation stimulating activity. It is not recommended for lactating mothers or for use in children.

Keywords: Feverfew; migraine; anti-inflammatory effects; rheumatoid arthritis



assessment report





1. Duke JA. Boca Raton, FL: CRC Press; 1985. CRC Handbook of Medicinal Herbs.
2. Jackson B, McDonald RL. Magic and Medicine of Plants. In: Dobelis IN, editor. Pleasantville, NY: Reader’s Digest Assoc; 1986.
3. Meyer JE. Hammond IN: Hammond Book Co; 1934. The Herbalist.
4. Chavez M, Chavez P. Hosp Pharm. 1999;34:436–61.
5. Jain NK, Kulkarni SK. J Ethnopharmacol. 1999;68:251–9.
6. Heptinstall S, Awang DW, Dawson BA, Kindack D, Knight DW. J Pharm Pharmacol. 1992;44:391–5.
7. Setty AR, Sigal AH. Semin Arthritis Rheum. 2005;34:773–84.
8. Pittler MH, Ernst E. Feverfew for preventing migraine. Cochrane Database Syst Rev. 2004;1:2286.
9. Sumner H, Salan U, Knight DW, Hoult JR. Biochem Pharmacol. 1992;43:2313–20.
10. Bohlmann F, Zdero C. Phytochemistry. 1982;21:2543–9.
11. Lancet. 1985;1:1084.
12. Johnson ES, Kadam NP, Hylands DM, Hylands PJ. Br Med J. 1985;291:569–73.
13. Waller PC, Ramsay LE. Br Med J. 1985;291:1128.
14. Murphy JJ, Heptinstall S, Mitchell JL. Lancet. 1988;2:189–92.
15. Groenewegen WA, Knight DW, Heptinstall S. Prog Med Chem. 1992;29:217–38.
16. Biggs MJ, Johnson ES, Persaud NP, Ratcliffe DM. Lancet. 1982;2:776.
17. Pfaffenrath V, Diener HC, Fischer M, Friede M, Zepelin HH. Cephalalgia. 2002;22:523–32.
18. Awang DV. Fever few: HerbalGram. 1993;29:34–5.
19. Losche W, Mazurov AV, Heptinstall S, Groenewegen WA, Repin VS, Till U. Thromb Res. 1987;48:511–8.
20. DeWeerdt C, Bootsma H, Hendriks H. Phytomedicine. 1996;3:225–30.
21. Pattrick M, Heptinstall S, Doherty M. Ann Rheum Dis. 1989;48:547–9.
22. Smith TH, Liu X. Cell Immunol. 2001;209:89–96.
23. Miller LG. Herbal medicinals: Arch Intern Med. 1998;158:2200–11.
24. Vickers HR. Br Med J. 1985;291:827.