Overview of Benefits
- Regenerates neuronal network (promotes the growth of both normal and damaged nerve cells)
- Inhibits the breakdown of acetylcholine
- Powerful antioxidant properties that seek and destroy the free radicals
- Promising alternative treatment for a variety of degenerative diseases such as Alzheimer’s and Parkinson’s
- Used to treat anxiety and depression
- Protects the brain against stress
- Improves sleep
Known as a revitalizing tonic for the brain and body, ashwagandha (Withania somnifera L. Dunalis) also a herb becoming recognized for its ability to enhance cognition and rebuild components of the neuronal network in damaged brains.
Inhibits the breakdown of acetylcholine. Acetylcholine is the chemical neurotransmitter in the brain which functions to optimize mental clarity and memory. This is important in those with DS, since according to "Understanding Down Syndrome Features" by Craig Stellpflug NDC, there are fewer acetylcholine receptors in the brain causing some of the memory and learning problems. A lack of acetylcholine also accounts for faulty communications in the endocrine system resulting in glandular and hormonal shortfalls.
Levels of acetylcholine can be raised by inhibiting the enzyme (acetylcholinesterase) which breaks down acetylcholine. Ashwagandha is a natural acetylcholinesterase inhibitor, and can increase levels of acetylcholine. The most commonly prescribed drugs for mental dementia also work on this principle.
Regeneration of neuronal network. Therapeutic and long lasting changes to damaged brains requires regeneration of the neuronal network. In mice which have suffered amlyoid induced neuron atrophy (as in Alzheimer’s disease), ashwagandha (as well as panax ginseng) were shown to regenerate axons, dendrites and reconstruct synapses in damaged neurons. The mice in these studies showed a significant improvement in memory function.
I like Organic India Ashwagandha in the capsules for us adults and the Sun Potions powder for Jett.
Ashwagandha is available in many forms and you need to follow different dosages for each. Jett takes 1/8 of a teaspoon of the powder in the morning. (He muscle tested as needing in more in the morning--maybe because it's calming and reduces daily stress-- than at night.) For adults who have ashwagandha powder, you may take 3 to 6 grams three times a day. My husband and I take it before bed but many people take it to give them energy in the morning. You should avoid taking ashwagandha if you are on any type of sedative medications.
Please comment if you have experience with giving it to your child.
What is Ashwagandha?
It's an exotic Indian herb, has remarkable stress-relieving properties comparable to those of powerful drugs used to treat depression and anxiety. In addition to its excellent protective effects on the nervous system, ashwagandha may be a promising alternative treatment for a variety of degenerative diseases such as Alzheimer’s and Parkinson’s. Ashwagandha has powerful antioxidant properties that seek and destroy the free radicals that have been implicated in aging and numerous disease states.
Powerful Protective Effects on the Nervous System
Stress, environmental toxins, and poor nutrition all have a detrimental impact on our nervous systems.
Scientific studies support ashwagandha’s ability not only to relieve stress, but also to protect brain cells against the deleterious effects of our modern lifestyles.
For example, in validated models of anxiety and depression, ashwagandha has been demonstrated to be as effective as some tranquilizers and antidepressant drugs. Specifically, oral administration of ashwagandha for five days suggested anxiety-relieving effects similar to those achieved by the anti-anxiety drug lorazepam (Ativan®), and antidepressant effects similar to those of the prescription antidepressant drug imipramine (Tofranil®).1
Stress can cause increased peroxidation of lipids, while decreasing levels of the antioxidant enzymes catalase and glutathione peroxidase. When ashwagandha extract was administered by re-searchers one hour before a daily stress-inducing procedure, all of the aforementioned parameters of free radical damage normalized in a dose-dependent manner.2 Premature aging associated with chronic nervous tension may be related to increased oxidative stress, which is abolished by the potent antioxidant properties of ashwagandha extract. Researchers believe this finding supports the clinical use of ashwagandha as an anti-stress agent.
Other studies of chronic stress support these findings. For example, in a remarkable animal study, examination of the brains of sacrificed animals showed that 85% of the brain cells observed in the animals exposed to chronic stress showed signs of degeneration. It is this type of cellular degeneration that can lead to long-term cognitive difficulties. Amazingly, when ashwagandha was administered to chronically stressed animals, the number of degenerating brain cells was reduced by 80%!3
In one of the most complete human clinical trials to date, researchers studied the effects of a standardized extract of ashwagandha on the negative effects of stress, including elevated levels of the stress hormone cortisol. Many of the adverse effects of stress are thought to be related to elevated levels of cortisol. The results were impressive. The participants subjectively reported increased energy, reduced fatigue, better sleep, and an enhanced sense of well-being. The participants showed several measurable improvements, including a reduction of cortisol levels up to 26%, a decline in fasting blood sugar levels, and improved lipid profiles. It would appear from this study that ashwagandha can address many of the health and psychological issues that plague today’s society.4
Over the past five years, the Institute of Natural Medicine at the Toyama Medical and Pharmaceutical University in Japan has conducted extensive research into the brain benefits of ashwagandha. The Institute’s scientists were looking for ways to encourage the regeneration of nerve cell components called axons and dendrites in validated models of the human brain. This important research may one day benefit those who have incurred brain injuries due to physical trauma, as well as those who suffer cognitive decline due to destruction of the nerve cell networks from diseases such as dementia and Alzheimer’s.
Using a validated model of damaged nerve cells and impaired nerve-signaling pathways, re-searchers noted that ashwagandha supported significant regeneration of the axons and dendrites of nerve cells. Furthermore, ashwagandha extract supported the reconstruction of synapses, the junctions where nerve cells communicate with other cells. The investigators concluded that ashwagandha extract helps to reconstruct networks of the nervous system, making it a potential treatment for neurodegenerative diseases such as Alzheimer’s.5
In another study at the same institute, researchers found that ashwagandha helped support the growth of nerve cell dendrites, which allow these cells to receive communications from other cells. This finding suggests that ashwagandha could help heal the brain tissue changes that accompany dementia.6
Finally, in a third published study, the researchers noted that ashwagandha helped promote the growth of both normal and damaged nerve cells, suggesting that the herb may boost healthy brain cell function as well as benefit diseased nerve cells.7
These findings provide tremendous hope that ashwagandha extracts may one day help heal neurodegenerative diseases in humans, freeing patients from the mental prisons of dementia and Alzheimer’s. Clearly, this is just the beginning of research into ashwagandha’s ability to encourage physical re-growth of the brain.
Ashwagandha also shows promise as a treatment for Parkinson’s and Alzheimer’s diseases, chronic neurodegenerative conditions for which there currently are no cures. In a recent study using a standardized model of human Parkinson’s disease, ashwagandha extract reversed all the parameters of Parkinson’s-type neurodegeneration significantly and in a dose-dependent manner.8 Remarkably, an earlier study showed that ashwagandha extract inhibits acetylcholinesterase, an enzyme responsible for breaking down one of the brain’s key chemical messengers. Drugs currently used in the treatment of Alzheimer’s disease, such as Aricept®, act in this very manner to slow the progression of this frightening, mind-robbing disease.9
1. Bhattacharya SK, Bhattacharya A, Sairam K, Ghosal S. Anxiolytic-antidepressant activity of Withania somnifera glycowithanolides: an experimental study. Phytomedicine. 2000 Dec;7(6):463-9.
2. Bhattacharya A, Ghosal S, Bhattacharya SK. Antioxidant effect of Withania somnifera glycowithanolides in chronic footshock stress-induced perturbations of oxidative free radical scavenging enzymes and lipid peroxidation in rat frontal cortex and striatum. J Ethnopharmacol. 2001 Jan;74(1):1-6.
3. Jain S, Shukla SD, Sharma K, Bhatnagar M. Neuroprotective effects of Withania somnifera Dunn. in hippocampal sub-regions of female albino rat. Phytother Res. 2001 Sep;15(6):544-8.
4. Unpublished study, 2005. NutrGenesis, LLC.
5. Kuboyama T, Tohda C, Komatsu K. Neuritic regeneration and synaptic reconstruction induced by withanolide A. Br J Pharmacol. 2005 Apr;144(7):961-71.
6. Tohda C, Kuboyama T, Komatsu K. Dendrite extension by methanol extract of Ashwagandha (roots of Withania somnifera) in SK-N-SH cells. Neuroreport. 2000 Jun 26;11(9):1981-5.
7. Tohda C, Kuboyama T, Komatsu K. Search for natural products related to regeneration of the neuronal network. Neurosignals. 2005;14(1-2):34-45.
8. Ahmad M, Saleem S, Ahmad AS, et al. Neuroprotective effects of Withania somnifera on 6-hydroxydopamine induced Parkinsonism in rats. Hum Exp Toxicol. 2005 Mar;24(3):137-47.
9. Choudhary MI, Yousuf S, Nawaz SA, Ahmed S, Atta uR. Cholinesterase inhibiting withanolides from Withania somnifera. Chem Pharm Bull (Tokyo). 2004 Nov;52(11):1358-61.
10. Govindarajan R, Vijayakumar M, Pushpangadan P. Antioxidant approach to disease management and the role of ‘Rasayana’ herbs of Ayurveda. J Ethnopharmacol. 2005 Jun 3;99(2):165-78.
11. Anon. Monograph. Withania somnifera. Altern Med Rev. 2004 Jun;9(2):211-4.
12. Owais M, Sharad KS, Shehbaz A, Saleemuddin M. Antibacterial efficacy of Withania somnifera (ashwagandha) an indigenous medicinal plant against experimental murine salmonellosis. Phytomedicine. 2005 Mar;12(3):229-35.
13. Davis L, Kuttan G. Immunomodulatory activity of Withania somnifera. J Ethnopharmacol. 2000 Jul;71(1-2):193-200.
14. Jayaprakasam B, Zhang Y, Seeram NP, Nair MG. Growth inhibition of human tumor cell lines by withanolides from Withania somnifera leaves. Life Sci. 2003 Nov 21;74(1):125-32.
15. Mathur R, Gupta SK, Singh N, et al. Evaluation of the effect of Withania somnifera root extracts on cell cycle and angiogenesis. J Ethnopharmacol. 2006 Jan 9.
16. Padmavathi B, Rath PC, Rao AR, Singh RP. Roots of Withania somnifera inhibit forestomach and skin carcinogenesis in mice. Evid Based Complement Alternat Med. 2005 Mar;2(1):99-105.
17. Mathur S, Kaur P, Sharma M, et al. The treatment of skin carcinoma, induced by UV B radiation, using 1-oxo-5beta, 6beta-epoxy-witha-2-enolide, isolated from the roots of Withania somnifera, in a rat model. Phytomedicine. 2004 Jul;11(5):452-60.
18. Christina AJ, Joseph DG, Packialakshmi M, et al. Anticarcinogenic activity of Withania somnifera Dunal against Dalton’s ascitic lymphoma. J Ethnopharmacol. 2004 Aug;93(2-3):359-61.
19. Gupta YK, Sharma SS, Rai K, Katiyar CK. Reversal of paclitaxel induced neutropenia by Withania somnifera in mice. Indian J Physiol Pharmacol. 2001 Apr;45(2):253-7.
20. Davis L, Kuttan G. Effect of Withania somnifera on cytokine production in normal and cyclophosphamide treated mice. Immunopharmacol Immunotoxicol. 1999 Nov;21(4):695-703.
21. Aphale AA, Chhibba AD, Kumbhakarna NR, Mateenuddin M, Dahat SH. Subacute toxicity study of the combination of ginseng (Panax ginseng) and ashwagandha (Withania somnifera) in rats: a safety assessment. Indian J Physiol Pharmacol. 1998 Apr;42(2):299-302.Emerging evidence also suggests that ashwagandha has anti-cancer benefits as well. Read more from: http://www.lef.org/magazine/mag2006/jun2006_report_ashwa_01.htm
Neuroprotective effects of Withania somnifera dunal.: A possible mechanism.
Bhatnagar M, Sharma D, Salvi M.
M.L. Sukhadia University, Udaipur, India. firstname.lastname@example.org
Present study was carried out to understand the possible mechanism of neuroprotective action of the root extract of Withania somnifera Dunal (WS). The study is focused on WS mediated inhibition of nitric oxide production, which is known to mediate neurodegeneration during stress. Adult mice (28 +/- 5 g) were exposed to restraint stress for 30 days. Activity of NADPH diaphorase (NADPH-d) and factors (Acetylcholine, serotonin and corticosterone), which regulates NADPH-d activity were studied. Treatment with WS extract for 30 days during stress, significantly reversed the stress induced NADPH-d activation. Observations suggest that inhibition of NADPH-d by WS is not a direct effect of extract on NADPH-d, instead it inhibits via suppressing corticosterone release and activating cholineacetyltransferase, which in turn increase serotonin level in hippocampus to inhibit NADPH-d. Together, the main mechanism underlying the neuroprotective effects of WS can be attributed to its role in the down regulation of nNOS and neurochemical alterations of specific neurotransmitter systems. These observations thus suggest that WS root extract could be developed as a potential preventive or therapeutic drug for stress induced neurological disorders.
J Ethnopharmacol. 2009 Sep 25;125(3):369-73. Epub 2009 Aug 8.
Withania somnifera root extract improves catecholamines and physiological abnormalities seen in a Parkinson's disease model mouse.
RajaSankar S, Manivasagam T, Sankar V, Prakash S, Muthusamy R, Krishnamurti A, Surendran S.
Department of Anatomy, Annamalai University, Tamilnadu, India.
ETHNOPHARMACOLOGICAL RELEVANCE: Withania somnifera root extract (Ws)/Ashwagandha/Indian ginseng is a traditional herbal medicine, used over 4000 years in India, shown to have effect on neural growth and locomotor function. Although catecholamines and oxidative stress resulting in neurodegeneration and locomotor disorder are the main events in Parkinson's disease (PD), efficacy of the drug on these molecules and physiological abnormality are not clear. AIM OF THE STUDY: The objective of the study was to examine effect of Ws on catecholamines and physiological abnormalities seen in PD using PD model mouse.
MATERIALS AND METHODS: Mouse were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 4 days to show biochemical and physiological abnormalities similar to patients with PD. PD mice were treated with Ws 100mg/kg body weight for 7 or 28 days. Catecholamines: dopamine (DA), 3,4-dihydroxy-phenylacetic acid (DOPAC) and homovanillic acid (HVA); antioxidants: glutathione (GSH) and glutathione peroxidase (GPx); and lipid peroxidation marker (TBARS) were analyzed in the Ws treated and untreated PD mouse striatum.
RESULTS: Mouse treated with MPTP showed reduced levels of DA, DOPAC, HVA, GSH and GPx and induced thiobarbituric acid reactive substance (TBARS) level compared to the control. Physiological abnormalities were seen in the mouse as determined by hang test and rotarod test. Oral treatment of PD mouse Ws root extract (100mg/kg body weight) for 7 days or 28 daysincreased DA, DOPAC and HVA levels and normalized TBARS levels in the corpus striatum of the PD mouse. The 7 days Ws treated mice showed improved motor function as determined by hang test and rotarod test. Treatment with Ws for 28 days increased GSH and GPx levels in the striatum compared to the Ws untreated PD mouse striatum.
CONCLUSION: These data suggest that Ws is a potential drug in treating catecholamines, oxidative damage and physiological abnormalities seen in the PD mouse.
Ashwagandha proven to be a potential cure for Alzheimers
Ashwagandha extract can reverse memory loss and could be a promising cure for Alzheimers in humans.
Neurochem Res. 2012 Sep;37(9):1915-27. doi: 10.1007/s11064-012-0810-5. Epub 2012 Jun 15.
Oxidative stress induced NMDA receptor alteration leads to spatial memory deficits in temporal lobe epilepsy: ameliorative effects of Withania somnifera and Withanolide A.
Soman S, Korah PK, Jayanarayanan S, Mathew J, Paulose CS.
Molecular Neurobiology and Cell Biology Unit, Department of Biotechnology, Centre for Neuroscience, Cochin University of Science and Technology, Cochin 682 022, Kerala, India.
In the present study we investigate the effect of Withania somnifera (WS) root extract and Withanolide A (WA) in restoring spatial memory deficit by inhibiting oxidative stress induced alteration in glutamergic neurotransmission. We demonstrate significant cellular loss in hippocampus of epileptic rats, visualized through decreased TOPRO stained neurons. Impaired spatial memory was observed in epileptic rats after Radial arm maze test. Treatment with WS and WA has resulted in increased number of TOPRO stained neurons. Enhanced performance of epileptic rats treated with WS and WA was observed in Radial arm maze test. The antioxidant activity of WS and WA was studied using superoxide dismutase (SOD) and Catalase (CAT) assays in the hippocampus of experimental rats. The SOD activity and CAT activity decreased significantly in epileptic group, treatment with WS and WA significantly reversed the enzymatic activities to near control. Real time gene expression studies of SOD and GPx showed significant up-regulation in epileptic group compared to control. Treatment with WS and WA showed significant reversal to near control. Lipid peroxidation quantified using TBARS assay, significantly increased in epileptic rats. Treatment with WS and WA showed significant reversal to near control. NMDA receptor expression decreased in epileptic rats. The treatment with WS and WA resulted in physiological expression of NMDA receptors. This data suggests that oxidative stress effects membrane constitution resulting in decreased NMDA receptor density leading to impaired spatial memory.
Treatment with WS and WA has ameliorated spatial memory deficits by enhancing antioxidant system and restoring altered NMDA receptor density.
Phytother Res. 2010 Oct;24(10):1567-74.
In vitro protective effects of Withania somnifera (L.) dunal root extract against hydrogen peroxide and β-amyloid(1-42)-induced cytotoxicity in differentiated PC12 cells.
Kumar S, Seal CJ, Howes MJ, Kite GC, Okello EJ.
Medicinal Plant Research Group, School of Agriculture, Food and Rural Development, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.
Withania somnifera L. Dunal (Solanaceae), also known as 'ashwagandha' in Sanskrit and as 'Indian ginseng', is used widely in Ayurvedic medicine as a nerve tonic and memory enhancer, with antiaging, antistress, immunomodulatory and antioxidant properties. There is a paucity of data on the potential neuroprotective effects of W. somnifera root, as traditionally used, against H(2)O(2)- and Aβ((1-42))-induced cytotoxicity which are current targets for novel approaches to treat dementia, especially dementia of the Alzheimer's type (AD). In this study, an aqueous extract prepared from the dried roots of W. somnifera was assessed for potential protective effects against H(2)O(2)- and Aβ((1-42))-aggregated fibril cytotoxicity by an MTT assay using a differentiated rat pheochromocytoma PC12 cell line. The results suggest that pretreatments of differentiated PC12 cells with aqueous extracts of W. somnifera root significantly protect differentiated PC12 cells against both H(2)O(2)- and Aβ((1-42))-induced cytotoxicity, in a concentration dependent manner. To investigate the compounds that could explain the observed effects, the W. somnifera extract was analysed by liquid chromatography-serial mass spectrometry and numerous withanolide derivatives, including withaferin A, were detected.
These results demonstrate the neuroprotective properties of an aqueous extract of W. somnifera root and may provide some explanation for the putative ethnopharmacological uses of W. somnifera for cognitive and other neurodegenerative disorders that are associated with oxidative stress.Copyright © 2010 John Wiley & Sons, Ltd.
We've all been taking ashwagandha and none of us have seen any adverse side effects. Although it is said that ashwagandha side effects are virtually non-existent, there are some side effects that have been observed in some individuals during case studies. These side effects of ashwagandha include:
- There is a slight elevation of body temperature after one week of use
- Irritation in the gastrointestinal system
- Development of small lesions and inflammation
- Vascular congestion
- Kidney diseases
- Heaviness in abdomen
Ashwagandha side effects have only short, vague evidences that are not very conclusive. Indian adults, as well as children have been using ashwagandha for centuries, without any major problems. You should always speak to your doctor before consuming ashwagandha.
Many herbalist have warned that individuals with certain conditions should avoid using ashwagandha. People suffering from diabetes, liver diseases, digestive disorders and ulcers should not take ashwagandha. Liquid ashwagandha tonics are prepared in sugar and/or alcohol. Therefore, people with alcohol problems should also avoid intake of ashwagandha.
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