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Ginkgo Biloba (available from numerous manufacturers and as a combination product), Bioginkgo, Gincosan, Ginexin Remind, Ginkai, Ginkoba, Ginkgo Go!, Ginkgold, Ginkgo Power, Ginkgoba, Ginkgo Leaf, Quanterra Mental Sharpness, Ginko Biloba Premium Extract, Gingko Biloba Extract, Activated Ginkgo, Nuveg Ginkgo Power, Time Release Ginkgo Power, Senior Ginkgo Power, Herbal Sure Maximum Strength Gingko Biloba
Medicinal Parts: The medicinal parts are the fresh or dried leaves, and the seeds separated from their fleshy outer layer.
Flower and Fruit: The tree flowers for the first time when it is between 20 and 30 years old. The flowers are dioecious. They are in the axils of the lower leaves of the current year's short shoots. The male flowering parts are attached to short catkins. The female flowers have longer pedicles and are at the end of a leafless branch. Fertilization occurs months after pollination by spermatozoids, although usually only one ovule is fully formed. The light green or yellowish seeds, incorrectly called fruit, later become fleshy and plumlike. They have a diameter of 2.5 to 3 cm, and each contains a two-edged edible nut.
Leaves, Stem, and Root: Ginkgo biloba is a 30- to 40-m high dioecious tree with a girth of about 4 m. The trees can live for hundreds of years. The bark is light to dark brown with rough grooves and reticulate fissures. The leaves are fan-shaped with bifurcated ribs. They are fresh green to golden yellow in autumn. The female trees are pointed and pyramid-shaped; the male trees are broad and sparer.
Characteristics: The seeds smell like butyric, capric, or valeric acid when ripe.
Habitat: Ginkgo is indigenous to China, Japan and Korea, and is also found in Europe and the U.S.
Production: The leaves are harvested either mechanically or by hand from plantations or in the wild. The leaves are then dried and pressed into balls. A dry extract from the dried leaf of Ginkgo biloba is manufactured using acetone/water and subsequent purification steps without addition of concentrates or isolated ingredients.
Other Names: Maidenhair-Tree
ACTIONS AND PHARMACOLOGY
Flavonoids (0.5-1.8%): including monosides, biosides and triosides of quercetin, isorhamnetins, 3-O- methylmyristicins, and kaempferol, to some extent estered with p-coumaric acid
Biflavonoides (0.4-1.9%): for example, amentoflavone, bilobetin, 5-methoxybilobetin, ginkgetin, isoginkgetin
Trilactonic diterpenes (0.06-0.23%): ginkgolide A, B, C
Trilactonic sesquiterpene bilabolids (0.04-0.2%)
Ginkgo has shown anti-inflammatory, cognitive-promoting, antioxidant, and vascular effects. Ginkgo has been proved ineffective in the treatment of cocaine-dependency, depression, multiple sclerosis, and ulcerative colitis. Ginkgo has proved effective against peripheral occlusive arterial disease (Schweizer & Hautmann, 1999). One recent study showed Ginkgo improved efficacy of and tolerability of 5-fluorouracil in colon cancer treatment (Hauns et al, 2001); the drug may inhibit some bacteria (Brun-Pascaud et al, 1997; Struillou et al, 1995; Atzori et al, 1993; Mourey et al, 1985). The use of Ginkgo in cardiovascular disease looks promising, but well-controlled trials are needed to determine its effectiveness. Ginkgo has demonstrated antioxidant activity, inhibition of platelet aggregation, enhancement of coronary blood flow, vasodilation, and a decrease in human blood pressure (Mahady, 2002). A small pilot, double blind, placebo-controlled study, demonstrated reductions in frequency of attacks in patients with Raynaud's disease who took Ginkgo biloba extract (Muir et al, 2002).
The anti-inflammatory effect of Ginkgo may be related to reduced eosinophil infiltration. Cognitive function may be improved by the antioxidant properties of Ginkgo. Ginkgo may act as a free radical scavenger. Although known to produce symptomatic improvement of dementia, no single mechanism of action has been identified. Glucocorticoid levels may be reduced by Ginkgo. Ginkgo may inhibit several enzymes, including catechol-O-methyl transferase, cytochrome P450 3A4, glycerol-3-phosphate dehydrogenase, and monoamine oxidase, although studies have been contradictory. Ginkgo may improve pancreatic beta cell function and insulin metabolism, and may inhibit serotonin uptake. Several mechanisms have been proposed by which Ginkgo may relax smooth muscle. Ginkgo inhibited platelet-activating factor. Gingko improves hemodynamic parameters, such as blood flow, by decreasing blood viscosity and erythrocyte aggregation.
Anti-inflammatory Effects: Intradermal administration of platelet-activating factor (PAF) induced a biphasic inflammatory response similar to that invoked by antigen challenge in sensitive individuals. Ginkgolides, especially ginkgolide B, antagonized this response. When given orally, ginkgolides reduced eosinophil infiltration in atopic patients given intracutaneous injections of PAF (Rosenblatt & Mindel, 1997; Della-Loggia et al, 1993). Ginkgolide B is a potent inhibitor of platelet-activating factor (PAF), which is important for the induction of arachidonate-independent platelet aggregation. Ginkgolide B blocks the binding of PAF to its receptor resulting in an antagonistic effect (Chung, 1987). This effect will inhibit PAF-induced bronchoconstriction and airway hyperactivity, along with T-lymphocyte proliferation and cytokine production. PAF induces inflammation and changes in vascular permeability (Wada et al, 1988; Braquet, 1987; Anon, 1986).
Antioxidant Effects: Ginkgo biloba exerts ischemic protective and antioxidant effects through the flavonoids. This occurs through a free scavenger action and prevention of lipid peroxidation. Lipid peroxidation is involved in producing tissue and vascular damage as well as neuronal loss, which may lead to dementia (Dorman, 1992; Koc, 1995; Otamiri, 1989). The herb also reduces neutrophil infiltration and increases blood flow to prevent the progression of dementia ischemia. The antioxidant and membrane-stabilizing activity increases cerebral hypoxia tolerance (Braquet & Hosford, 1991; Koltringer, 1989; Otamiri, 1989).
Multiple mechanisms of action have been proposed for the action of Ginkgo biloba in the treatment of cerebral hypoxia. Ginkgolide B, a potent antagonist of PAF, decreased glycine levels in rats after brain injury, decreased PAF-induced increases in intracellular calcium (2+) levels, attenuated the activation of protein kinase C, and reduced excitatory amino acid receptor function. Other constituents of Ginkgo biloba may protect neurons by acting as oxygen radical scavengers. Ginkgo, acting on the hepatic cytochrome P-450 enzyme system, may also attenuate oxygen-free radical formation and the release of superoxide anions. Ginkgo may also increase the number of H(3)rauwolscine binding sites in the hippocampus as seen in aged rats. This effect could compensate for the declining number of alpha-adrenoreceptors, characteristic of aging. Ginkgo also inhibited catechol-O-methyl transferase and enhanced the vasoregulatory effect of catecholamines (Logani et al, 2000).
Ginkgo may be a free radical scavenger and prevent lipid peroxidation in a dose-dependent manner. This action protects vascular walls (Barth et al, 1991; Pincemail et al, 1989). It may also increase the half-life of endothelium-based relaxing factor by its free radical scavenging action on superoxide anions (thus relaxing contracted blood vessels) (Robak & Gryglewski, 1988). Animal studies demonstrate that Ginkgo also scavenges peroxyl radicals, which are involved in lipid peroxidation (Maitra et al, 1995).
Arteriosclerosis: Ginkgo may reduce arteriosclerotic lesions but human trials are needed. Arteriosclerosis leading to stroke developed more often in untreated rats than in rats treated with Tanakan[R], a preparation of Ginkgo biloba (Fang et al, 2000). Ginkgo extract (containing 24% ginkgoflavonglycosides) demonstrated a protective effect against oxidation of LDL to oxysterols in a study using human LDL. Oxysterols are highly cytotoxic and through macrophage scavengers create "foam cells" which are seen early in atheroma lesions (Rasetti et al, 1997).
Cognitive Function: The majority of studies have demonstrated a benefit with Ginkgo supplementation on cognition. Ginkgo demonstrated a benefit in elderly patients with mild to moderate memory impairment. At least 12 weeks of Ginkgo treatment is necessary before improvement occurs. Ginkgo slowed the rate of deterioration in severe dementia. Noncognitively impaired elderly adults may benefit from Ginkgo. Ginkgo did not enhance memory in young adults.
In dementia due to neuronal loss and impaired neurotransmission, there is a decrease in oxygen and glucose and a release of free radicals and lipid peroxidation (Kleijnen & Knipschild, 1992). The active ingredients in Ginkgo, the flavonoids (ginkgo-flavone glycosides) and terpenoids (ginkgolides and bilobalide), probably affect the progression of dementia in several ways, such as reducing neutrophil infiltration and lipid peroxidation (Otamiri & Tagesson, 1989), increasing blood flow (Koltringer et al, 1989), antagonizing platelet-activating factor (Wada et al, 1988), and changing neuron metabolism (DeFeudis, 1991; Hofferberth, 1991).
Radiolabeled rauwolscine binding to alpha-2-adrenoceptors in the cerebral cortex and hippocampus membranes was enhanced (28%) by Ginkgo extracts …