GINKGO (GINKGO BILOBA)
Ginkgo biloba extract
is prepared from the leaves of the ginkgotree. The most common formulation is
prepared by concentrating 50 parts of the crude leaf to prepare one part of
extract. The active constituents in ginkgo are flavone glycosides and
terpenoids (ie, ginkgolides A, B, C, J, and bilobalide).
In animal models and
some human studies, ginkgo has been shown to increase blood flow, reduce blood
viscosity, and promote vasodilation, thus enhancing tissue perfusion.
Enhancement of endogenous nitric oxide
and antagonism of platelet-activating factor have been observed in
animal models.
Ginkgo biloba has been
studied for its effects on mild to mod-erate occlusive peripheral arterial
disease. Among 11 randomized, placebo-controlled studies involving 477
participants using stan-dardized ginkgo leaf extract (EGb761) for up to 6
months, a nonsignificant trend toward improvements in pain-free walking
distance (increase of 64.5 meters) was observed (p = .06).
The Ginkgo Evaluation
of Memory (GEM) study evaluated cardiovascular outcomes associated with the
long-term use of ginkgo for 6 years in 3069 patients over 75 years of age.
Daily use of 240 mg/d EGb761 did not affect the incidence of hypertension or
reduce blood pressure among persons with hypertension or prehypertension. No
significant effects in cardiovascular disease
mortality
or events or hemorrhagic stroke were observed. There was, however, a
significant reduction in peripheral vascular disease events in the ginkgo arm
versus the placebo arm.
Antioxidant
and radical-scavenging properties have been observed for the flavonoid fraction
of ginkgo as well as some of the terpene constituents. In vitro, ginkgo has
been reported to have superoxide dismutase-like activity and superoxide anion-
and hydroxyl radical-scavenging properties. The flavonoid fraction has also
been observed to have anti-apoptotic properties. In some studies, it has also
dem-onstrated a protective effect in limiting free radical formation in animal
models of ischemic injury and in reducing markers of oxida-tive stress in
patients undergoing coronary artery bypass surgery.
In aged animal models,
chronic administration of ginkgo for 3–4 weeks led to modifications in central
nervous system recep-tors and neurotransmitters. Receptor densities increased
for mus-carinic, α2, and 5-HT1a receptors and decreased for β adrenoceptors.
Increased serum levels of acetylcholine and norepinephrine and enhanced
synaptosomal reuptake of serotonin have also been reported. Additional effects
include reduced corticosterone syn-thesis and inhibition of amyloid-beta fibril
formation.
Ginkgo has been used
to treat cerebral insufficiency and demen-tia of the Alzheimer type. The term cerebral insufficiency, however,
includes a variety of manifestations ranging from poor concentra-tion and
confusion to anxiety and depression as well as physical complaints such as
hearing loss and headache. For this reason, studies evaluating cerebral
insufficiency tend to be more inclusive and difficult to assess than trials
evaluating dementia. An updated meta-analysis of ginkgo for cognitive
impairment or dementia was performed by the Cochrane Collaboration. They
reviewed 36 ran-domized, double-blind, placebo-controlled trials ranging in
length from 3 to 52 weeks. Significant improvements in cognition and activities
of daily living were observed at 12 but not 24 weeks. Significant improvements
in clinical global improvement, however, were observed at 24 but not 12 weeks.
The authors concluded that the effects of ginkgo in the treatment of cognitive
impairment and dementia were unpredictable and unlikely to be clinically
relevant. In the GEM study, the effects of gingko as a prophylactic agent to
prevent progression to dementia were assessed. No benefit was observed with 6
years of ginkgo treatment. To date, there is no known therapy that prevents
progression to dementia.
Ginkgo
has been studied for its effects in allergic and asthmatic bronchoconstriction,
short-term memory in healthy, non-demented adults, erectile dysfunction,
tinnitus and hearing loss, and macular degeneration. For each of these
conditions, there is insufficient evidence to warrant clinical use.
Adverse
effects have been reported with a frequency comparable to that of placebo.
These include nausea, headache, stomach upset,diarrhea, allergy, anxiety, and insomnia. A
few case reports noted bleeding complications in patients using ginkgo. In a
few of these cases, the patients were also using either aspirin or warfarin.
Ginkgo may have
antiplatelet properties and should not be used in combination with antiplatelet
or anticoagulant medications. One case of an enhanced sedative effect was
reported when ginkgo was combined with trazodone. Seizures have been reported
as a toxic effect of ginkgo, most likely related to seed contamination in the
leaf formulations. Uncooked ginkgo seeds are epileptogenic due to the presence
of ginkgotoxin. Ginkgo formulations should be avoided in individuals with
preexisting seizure disorders.
Ginkgo biloba dried leaf extract is usually standardized to contain24% flavone
glycosides and 6% terpene lactones. The daily dose ranges from 120 to 240 mg of
the dried extract in two or three divided doses.
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