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Feverfew
Tanacetum parthenium |
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A chrysanthemum species used as a remedy for
migraines, headaches, fevers, & arthritis |
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| This strongly aromatic
perennial chrysanthemum, a species of the Asteraceae family, has been
used for treating fevers, headaches,arthritis, rheumatism, and menstrual
disorders since the time of Dioscorides (circa 78 A.D.) The leaves are
yellowish-green in color and pinnatesect in ovate segments, subdivided
into entire or crenate lobes. The plant’s flower grows with five to
twenty flowerheads in a dense corymb, with capitulums of yellow tubular
flowers and white ligulate, female flowers. The ray florets are up to 7
mm in length. The name chrysanthemum is from the Greek word chrys,
meaning golden, and the Latin word anthemum, meaning flower. The
common name feverfew is a corrupted version of the Latin febrifugia,
meaning fever reducer. The name parthenium comes from the Greek,
parthenos, meaning virgin, in reference to young women who used the
plant to treat menstrual irregularities. The principal active
constituent of feverfew is a sesquiterpenoid lactone called parthenolide.
Other sesquiterpenoid lactones present in feverfew and known to possess
pharmacological activity include canin, epoxy-artemorin, artecanin,
tanaparthin-a-peroxide,
and seco-tanapartholides A & B. The chemical composition of the plant
appears to fluctuate qualitatively depending on the origin of the plant
and its vegetative cycle. The parthenolide content is concentrated in
the flowering tops and the leaves. The plant also contains various
flavonoids and polyynes. The strong odor of feverfew is due to an
essential oil consisting of camphor, camphene, germacrene D, p-cymene,
linalool, borneol, and chrysanthemyl acetate. It has been demonstrated
through animal studies that feverfew extracts inhibit platelet
aggregation and the ADP- or epinephrine-induced release of serotonin, as
well as decreasing prostaglandin synthesis and the release of
inflammatory compounds called histamines. Feverfew reduces the release
of serotonin from thrombocytes and polymorphonuclear leukocytes.
Compounds such as parthenolide are called spasmolytic, meaning that they
cause the smooth muscles in the walls of the cerebral blood vessels to
be less reactive to endogenous chemicals such as norepinephrine,
prostaglandins, and serotonin which cause vasoconstriction and
inflammation. The body reacts to this vasoconstriction by releasing
autocoids, which are anti-inflammatory compounds with vasodilating
properties which counteract the vasoconstriction and inflammation. The
pain receptors which are activated during migraine headaches are wrapped
around the cerebral blood vessels and receive pressure from the
vasoconstriction-vasodilation activity resulting in a throbbing migraine
headache. Thus feverfew acts in a similar manner as a seronin
antagonist, preventing the serotonin dumping which triggers the initial
vasoconstriction and resultant vasodilation that leads to activation of
the pain receptors of the cerebral blood vessels. Another mechanism of
action is presumed to be the inhibition of arachidonic acid, a precursor
to prostaglandins that are involved in clotting mechanisms as well as
inflammatory responses. Extracts of feverfew also contribute a
protective effect on vascular endothelial cells. Due to its inhibitory
effect on platelet aggregation and arachidonic acid, feverfew should not
be taken in conjunction with anticoagulant medications or prior to
surgery. Feverfew should not be taken by pregnant or lactating women.
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