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Indian Ginseng
Ashwagandha
Promotes Energy, Mental Health, & Sexual Energy
Price range: 1-2 containers: $10.95 each. 3-5: $9.95 6+: $8.95
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Quality Assurance: This product is manufactured in the United States by one of America's leading laboratories in business since 1955. It is produced from natural sources and contains no yeast, sugar, starch, artificial flavor, dyes, coloring agent or preservatives.
See also: Korean Ginseng
Indian Ginseng is used to boost energy, improve mental capacity, and increase stamina, vitality, and sexual energy. It has been used in traditional Indian medicine for thousands of years as a “cure-all.”
It is not a direct relative of the Asian and American ginseng plants, but its uses are so similar that the name of the more well-known Chinese plant has been commonly adopted. Its traditional name is Ashwagandha.
Recent research has discovered the chemical processes behind the traditional uses of Indian Ginseng. The root of the plant contains flavonoids, saponins, and substances called withanolides. Flavonoids are antioxidant, anti-allergenic, and anti-inflammatory agents which are beneficial to overall good health. Saponins are plant steroids found in all plants and which boost the immune response. Withanolides provide the specific benefits of Indian Ginseng by reacting with neurotransmitters in the brain and increasing the concentration of acetylcholine, a chemical neurotransmitter. Together these substances promote a healthy environment in the nervous system and an optimal use of energy.
Supplement Facts:
Serving Size: 1 capsule
Servings Per Container: 60
Ashwagandha root & leaf 300mg
(Indian Ginseng, Withania somnifera)
Standardized to 1.5% With anolides
and 1% Alkaloids
Other ingredients: Gelatin (capsule), cellulose and vegetable stearate.
Quality Assurance: This product is produced under Good Manufacturing Practices and contains no wheat gluten, milk/dairy, corn, sodium, sugar, starch, artificial coloring, flavoring or preservatives.
Recommended Dosage:
Adults take 1 capsule daily or as directed by physician.
BACKGROUND:
Although it is often called “Indian ginseng”, Ashwagandha is not related to panax ginseng (“Chinese ginseng”), an unrelated species of herb. Ashwagandha acquired the name Indian Ginseng because it is used in the same way as Chinese ginseng, and it exhibits similar health benefits.
The “cure-all” reputation of ginseng derives from its cumulative effect on the body – it helps the body adapt to abnormal stresses such as fatigue and disease. For this reason it is labeled an adaptogen – a substance which helps restore balance and normalize the body’s functioning. Indian ginseng is an ancient means of maintaining good overall health.
By Ray Sahelian, MD:
Ashwagandha - also known as Indian Winter Cherry - is a shrub cultivated in India and North America whose roots have been used for thousands of years by Ayurvedic practitioners. Ashwagandha root contains flavonoids and many active ingredients of the withanolide class. Several studies over the past few years have looked into whether ashwagandha has anti-inflammatory, anti-tumor, anti-stress, antioxidant, mind-boosting, immune-enhancing, and rejuvenating properties (see studies at bottom of page). Historically ashwagandha root has also been noted to have sex-enhancing properties.
Ashwagandha (Withania somnifera) is an herb that is extensively used in Ayurveda, the traditional health care system in India. Ashwagandha is used as a general tonic and "adaptogen", helping the body adapt to stress. In addition, Ashwagandha has been shown to possess antioxidant activity as well as an ability to support a healthy immune system.
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CITATIONS:
“Systemic administration of defined extracts from Withania somnifera (Indian Ginseng) and Shilajit differentially affects cholinergic but not glutamatergic and GABAergic markers in rat brain”
by Schliebs R, Liebmann A, Bhattacharya SK, Kumar A, Ghosal S, Bigl V. Paul Flechsig Institute for Brain Research, Department of Neurochemistry, University of Leipzig, Germany. Neurochem Int 1997 Feb;30(2):181-90
ABSTRACT
Although some promising results have been achieved by acetylcholinesterase inhibitors, an effective therapeutic intervention in Alzheimer's disease still remains an important goal. Sitoindosides VII-X, and withaferin-A, isolated from aqueous methanol extract from the roots of cultivated varieties of Withania somnifera (known as Indian Ginseng), as well as Shilajit, a pale-brown to blackish brown exudation from steep rocks of the Himalaya mountain, are used in Indian medicine to attenuate cerebral functional deficits, including amnesia, in geriatric patients. The present investigation was conducted to assess whether the memory-enhancing effects of plant extracts from Withania somnifera and Shilajit are owing to neurochemical alterations of specific transmitter systems. Therefore, histochemistry to analyse acetylcholinesterase activity as well as receptor autoradiography to detect cholinergic, glutamatergic and GABAergic receptor subtypes were performed in brain slices from adult male Wistar rats, injected intraperitoneally daily with an equimolar mixture of sitoindosides VII-X and withaferin-A (prepared from Withania somnifera) or with Shilajit, at doses of 40 mg/kg of body weight for 7 days.
Administration of Shilajit led to reduced acetylcholinesterase staining, restricted to the basal forebrain nuclei including medial septum and the vertical limb of the diagonal band. Systemic application of the defined extract from Withania somnifera, however, led to differential effects on AChE activity in basal forebrain nuclei: slightly enhanced AChE activity was found in the lateral septum and globus pallidus, whereas in the vertical diagonal band AChE activity was reduced following treatment with sitoindosides VII-X and withaferin-A. These changes were accompanied by enhanced M1-muscarinic cholinergic receptor binding in lateral and medial septum as well as in frontal cortices, whereas the M2-muscarinic receptor binding sites were increased in a number of cortical regions including cingulate, frontal, piriform, parietal and retrosplenial cortex. Treatment with Shilajit or the defined extract from Withania somnifera affected neither GABAA and benzodiazepine receptor binding nor NMDA and AMPA glutamate receptor subtypes in any of the cortical or subcortical regions studied.
The data suggest that Shilajit and the defined extract from Withania somnifera affect preferentially events in the cortical and basal forebrain cholinergic signal transduction cascade. The drug-induced increase in cortical muscarinic acetylcholine receptor capacity might partly explain the cognition-enhancing and memory-improving effects of extracts from Withania somnifera observed in animals and humans.
http://nootropics.com/indianginseng/index.html
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Research:
“Effect of BR-16A (Mentat), a polyherbal formulation on drug-induced catalepsy in mice.”
Kumar,-A; Kulkarni,-S-K Citation: Indian-J-Exp-Biol. 2006 Jan; 44(1): 45-8
Parkinson's disease (PD) is a neurodegenerative disease characterized by the selective loss of dopamine (DA) neurons of the substantia nigra pars compacta (SNc). The events, which trigger and/or mediate the loss of nigral DA neurons, however, remain unclear. Neuroleptic-induced catalepsy has long been used as an animal model for screening drugs for Parkinsonism. Administration of haloperidol (1 mg/kg, ip) or reserpine (2 mg/kg, ip) significantly induced catalepsy in mice. BR-16A (50 and 100 mg/kg, po), a polyherbal formulation or ashwagandha (50 and 100 mg/kg, po), significantly reversed the haloperidol or reserpine-induced catalepsy. The results indicate that BR-16A or ashwagandha has protective effect against haloperidol or reserpine-induced catalepsy and provide hope that BR-16A could be used in preventing the drug-induced extrapyramidal side effects and may offer a new therapeutic approach to the treatment of Parkinson's disease.
“Selective Th1 up-regulating activity of Withania somnifera aqueous extract in an experimental system using flow cytometry.”
Bani,-S; Gautam,-M; Sheikh,-F-A; Khan,-B; Satti,-N-K; Suri,-K-A; Qazi,-G-N; Patwardhan,-B Citation: J-Ethnopharmacol. 2006 Aug 11; 107(1): 107-15
Withania somnifera (Ashwagandha) is reported to be immunoprotective and immunoadjuvant. We studied its roots aqueous extract on T helper (Th) immunity using flow cytometry. This extract was standardized with six withanolides as marker compounds using HPLC. Once daily dose ranging from 25 to 400 mg/kg/p.o. was used to study effect on Th1: IFN-gamma, IL-2 and Th2: IL-4 cytokine modulation. We also studied effect on CD4 and CD8 in normal and immunesuppressed mice. The results indicate that extract at 100 mg/kg resulted significant selective up-regulation of Th1 response. Treatment with extract showed significant increase in CD4 and CD8 counts as compared to control and cyclopsorin A, with a faster recovery of CD4+ T cells in immunesuppressed animals. Under immunesuppressed conditions, potentiation of cellular and humoral immune responses of extract was comparable to levamisole. This study indicates the selective Th1 up-regulating effect of extract and suggests its use for selective Th1/Th2 modulation.
“Antibacterial efficacy of Withania somnifera (ashwagandha) an indigenous medicinal plant against experimental murine salmonellosis.”
Owais,-M; Sharad,-K-S; Shehbaz,-A; Saleemuddin,-M Citation: Phytomedicine. 2005 Mar; 12(3): 229-35
In the present study, we evaluated the antibacterial activity of ashwagandha [Withania somnifera L. Dunal (Solanaceae; root and leaves)], an Indian traditional medicinal plant against pathogenic bacteria. Both aqueous as well as alcoholic extracts of the plant (root as well as leaves) were found to possess strong antibacterial activity against a range of bacteria, as revealed by in vitro Agar Well Diffusion Method. The methanolic extract was further subfractionated using various solvents and the butanolic sub-fraction was found to possess maximum inhibitory activity against a spectrum of bacteria including Salmonella typhimurium. Moreover, in contrast to the synthetic antibiotic (viz. chloramphenicol), these extracts did not induce lysis on incubation with human erythrocytes, advocating their safety to the living cells. Finally, the antibacterial efficacy of the extracts isolated from plant (both root and leaves) was determined against experimental salmonellosis in Balb/C mice. Oral administration of the aque ous extracts successfully obliterated salmonella infection in Balb/C mice as revealed by increased survival rate as well as less bacterial load in various vital organs of the treated animals.
“Search for natural products related to regeneration of the neuronal network.”
Tohda,-C; Kuboyama,-T; Komatsu,-K Citation: Neurosignals. 2005; 14(1-2): 34-45
The reconstruction of neuronal networks in the damaged brain is necessary for the therapeutic treatment of neurodegenerative diseases. We have screened the neurite outgrowth activity of herbal drugs, and identified several active constituents. In each compound, neurite outgrowth activity was investigated under amyloid-beta-induced neuritic atrophy. Most of the compounds with neurite regenerative activity also demonstrated memory improvement activity in Alzheimer's disease-model mice. Protopanaxadiol-type saponins in Ginseng drugs and their metabolite, M1 (20-O-beta-D-glucopyranosyl-(20S)-protopanaxadiol), showed potent regeneration activity for axons and synapses, and amelioration of memory impairment. Withanolide derivatives (withanolide A, withanoside IV, and withanoside VI) isolated from the Indian herbal drug Ashwagandha, also showed neurite extension in normal and damaged cortical neurons. Trigonelline, a constituent of coffee beans, demonstrated the regeneration of dendrites and axons, in addition to memory improvement. 2005 S. Karger AG, Basel
“Induction of nitric oxide synthase expression by Withania somnifera in macrophages.”
Iuvone, T : Esposito, G : Capasso, F : Izzo, A A Citation: Life-Sci. 2003 Feb 21; 72(14): 1617-25
Withania somnifera (ashwagandha, Indian ginseng) is an immunostimulant herbal medicine used to improve overall health and prevent diseases, particularly in the elderly. However, the mechanisms underlying its immunostimulant effect is poorly understood. To elucidate the mechanism of Withania somnifera, we investigated the effect of a methanolic extract from the root of Withania somnifera (WS) on nitric oxide (NO) production in J774 macrophages. We found that WS (1-256 microg/ml) produced a significant and concentration-dependent increase in NO production, an effect which was abolished by N(G)nitro-L-arginine methyl ester (L-NAME, 3-300 microM), a non-selective inhibitor of NO synthase (NOS), dexamethasone (10 microM), an inhibitor of protein synthesis and N(alpha-p)-tosyl-L-lysine chloromethyl ketone (TLCK, 0.01-10 microM), an inhibitor of nuclear factor-kappaB (NF-kappaB) activation. Dexamethasone did not have any effect on NO production once NOS had been induced (i.e. 12 h after WS). Moreover, western blot analysis showed that WS increased, in a concentration-dependent fashion, inducible NOS protein expression. These results demonstrate that WS may induce the synthesis of inducible NOS expression likely by acting at transcriptional level. The increased NO production by macrophages could account, at least in part, for the immunostimulant properties of Withania somnifera.
“Adaptogenic and cardioprotective action of ashwagandha in rats and frogs.”
Dhuley, J N Citation: J-Ethnopharmacol. 2000 Apr; 70(1): 57-63
Pharmacological and metabolic effects of ashwagandha (Withania somnifera L. (Solanaceae)) used in Ayurveda as a herbal tonic and health food were studied. Ashwagandha was shown to increase swimming time in rats in physical working capacity test, i.e. rats swimming endurance test. Significant increase in relative heart weight and glycogen content in myocardium and liver was also observed in ashwagandha treated group. Ashwagandha treatment increased the duration of contractility in functional test for the resistance of frog heart muscle towards the toxic action of strophanthin-K. Ashwaaandha treatment also resulted in significant increase in coagulation time which attains normalcy 7 days after cessation of treatment. Ashwagandha possesses no toxicity up to a dose of (100 mg/kg; p.o. for 180 days) and does not cause significant changes in biochemical parameters in the blood serum of rats. Increase in catecholamine content in the heart and aortic tissues and their decrease in adrenal glands are unfavourable effects of high doses of ashwagandha. On the basis of these observations, it was concluded that ashwagandha possesses adaptogenic, cardiotropic, cardioprotective and anticoagulant properties.
“Dendrite extension by methanol extract of Ashwagandha (roots of Withania somnifera) in SK-N-SH cells.”
Tohda, C : Kuboyama, T : Komatsu, K Citation: Neuroreport. 2000 Jun 26; 11(9): 1981-5
Extension of dendrites and axons in neurons may compensate for and repair damaged neuronal circuits in the dementia brain. Our aim in the present study was to explore drugs activating neurite outgrowth and regenerating the neuronal network. We found that the methanol extract of Ashwagandha (roots of Withania somnifera; 5 microg/ml) significantly increased the percentage of cells with neurites in human neuroblastoma SK-N-SH cells. The effect of the extract was dose- and time-dependent mRNA levels of the dendritic markers MAP2 and PSD-95 by RT-PCR were found to be markedly increased by treatment with the extract, whereas those of the axonal marker Tau were not. Immunocytochemistry demonstrated the specific expression of MAP2 in neurites extended by the extract. These results suggest that the methanol extract of Ashwagandha promotes the formation of dendrites.
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The statements & claims found on this website have not been
evaluated by the Food & Drug Administration.
These products are not intended to diagnose, treat, cure, or prevent any disease.
© Copyright 2006, 2007, by Good Health Group of America, LLC.
311 Bainbridge Street, Philadelphia PA USA 19147.
www.GoodHealthCo.com
Indian ginseng available from Good Health Group of America
.
The statements & claims found on this website have not been evaluated by the Food & Drug Administration.
These products are not intended to diagnose, treat, cure, or prevent any disease.
© Copyright 2006, 2007, by Good Health Group of America, LLC.
311 Bainbridge Street, Philadelphia PA USA 19147.
www.GoodHealthCo.com
