Aswhagandha, or Withania somnifera (L) Dunal is a widely cultivated plant in India of the Solanaceae family (which includes the common tomato and potato). In the wild, it occurs mainly in the Indian subcontinent, Central Asia and the Middle East. Ashwagandha has been used for thousands of years in traditional Ayurvedic medicine and, as with Bacopa monnieri, it is classified as Medhya Rasayana – meaning it rejuvenates, brings clarity and peace of mind. Its name in Sanskrit translates into „horse smell,” which is due to the plant's characteristic odor as well as the belief that it can give the strength and vitality of a horse.1,2 The medical resource is, above all, the root of the herb, from which extracts containing mainly glycosidic sitoindosides and steroidal lactones (withanolides) are obtained. In terms of chemical structure, withanolides resemble the active substances of the Panax ginseng root, which is why Ashwagandha is commonly referred to as Indian Ginseng. In ayurvedic medicine, it is used in the treatment of rheumatism, memory loss, general fatigue and impotence.2,3
Withania somnifera, as well as its extracts, have a characteristic and complex effect on the functioning of our nervous system. This includes its adaptogenic, anti-depressant, and anxiolytic effects, which leads to reduced stress levels and improvement in mood.2 As with benzodiazpines, Ashwagandha modulates GABA system activity, and its anxiolytic effect is comparable to diazepam and imipramine.4 Both its Latin and Polish names relate to its effects on sleep quality. Studies have shown that this plant helps to restore disregulated circadian sleep deficiency.5
Moreover, studies using experimental models of acute seizures and chronic models of epilepsy demonstrated the anticonvulsant effects of withanolides. These compounds, in combination with standard anti-epileptic medication, allow for a significant dose reduction of the latter without inhibiting the effectiveness of therapy, which in turn results in a higher safety level and lower mortality rate of those undergoing treatment.2
Prolonged stress leads to elevated levels of corticosteroids and as a consequence, to excessive production of nitric oxide (NO); which, in the right concentration, facilitates the release of many neuro-transmitters, including GABA, and also plays an important role in synpatic plasticity and development of nerve cells. These processes occur within practically the entire central nervous system and their proper course in the hippocampus, the cortex and the basal ganglia is of crucial importance to cognitive and emotional reactions. NO easily reacts with superoxide (O2 • -) arising during cell respiration, as a result of this reaction produces peroxynitrite (ONOO-), which is toxic to nerve cells.
Studies have shown that Withania S. root extracts reduce the release of corticosteroids and lead to a reduced activity of the enzymes responsible for the production of nitric oxide.6 Moreover, withanolides and sitoindosides (VII-X) increase the activity of the enzymes responsible for the decomposition and disposal of reactive oxygen. They prevent oxidation of lipids included in the cell membrane thanks to which they protect against neurodegenerative diseases, such as Alzheimer's or Parkinson's disease and dyskinesia - involuntary contractions of the muscles associated with the use of classical neuroleptics.6,7
A high level of corticosteroids is related to stress and has a negative impact on the proper functioning of the acetylcholine and serotonin systems. By reducing the levels of „stress hormones,” Ashwagandha leads to the normalization of serotonin transmission, and also increases the sensitivity of 5-HT2 receptors.6,8 In the case of the acetylcholine system, Ashwagandha increases the activity of the enzymes responsible for the synthesis of this choline derivative while simultaneously inhibiting the activity of acetylcholinesterase- the enzyme thatbreaks down acetylcholine.9,10
Thanks to these properties, Ashwagandha improves memory, cognitive processes and improves mood. Moreover, it may be a potential alternative to conventional treatments of Alzheimer's disease.2,6,9,10
A rational argument for the belief in the "horse health" which is attributed to Ashwagandha may be the fact that both the full extract of this herb and cleaned withanolide A increase cell proliferation of the immune system (such as B and T cells) when it encounters a pathogen.11 A similar effect was observed int he case of neutrophil, whose activation after an 8-day treatment with withanolide extract was comparable to intravenal administration of GM-CSF- a cytokine that takes part in hemogenesis. This is why Ashwagandha use is especially recommended for individuals diagnosed with neutropenia.12
Additionally, in contrast to the afore-mentioned immuno-stimulating properties, Ashwagandha also shows to have anti-inflammatory effects. Withaferin A, found in the plant's extracts, decreases the release and activity of pro-inflammatory cytokines, such as the soluble form of the tumor necrosis factor (TNF) and interleukin-1 β, which is responsible for the development of arthritis and multiple auto-inflammatory syndromes .13
The anti-oxidant properties of the compounds found in Withania s. are not limited only to the nervous system, but also protect all of the cells of the body from oxidative stress, which is the herb has a preventive effect in the case of various types of cancer.13 Moreover, Ashwagandha also works well as a natural adjuvant to conventional cancer therapy. Studies have shown that witahaferin A suppresses the formation of new and existing blood vessels, thus reduceing the possibility of tumor growth and kills its cells by induction of apoptosis, or controlled tumor cell suicide. It also reduces the amount of adhesion molecules on the cell surface thereby reducing the ability of tumor cells to metastasize.13,14
In the case of the extract standardized to 5% content of withanolides, the effects can be felt when taking 50 mg of extract per day. An optimal daily dose is 100 mg. Studies have used doses from 200-400 mg. A larger daily dose is best when divided into 2-3 smaller doses, and taken after meals.15
To achieve the best anti-stress and pro-cognitive results, it is very beneficial to combine Ashwagandha with curcumin, silymarin and Valerian products (Valeriana officinalis), Bacopa monnieri or martyrs (Passiflora L.), and other supplements containing 5-HTP, L theanine or EGCG. If the purpose of supplementation is to enhance libido and body condition, it is recommended to use this herb together with the mountain Rhodiola (Rhodiola rosea), Tribulus terrestris, matzah (Lepidium meyenii), epimedium, Tongkat Ali, Terminalia arjuna or eleuthero.
Do not combine with alcohol, antidepressants, hypnotics, anesthetics, and antiepileptic drugs without prior consultation with your doctor.
Ashwagandha is considered safe and can be used as a therapeutic agent for various diseases. Side effects may occur very rarely. These include nasal congestion (rhinitis), constipation, cough and cold, sleepiness, and decreased appetite.1,13
The product has been tested for toxicity in pregnant women and the fetus. No changes were detected in both mother and child. Nevertheless, for safety reasons, the preparation should not be used by pregnant and breastfeeding women.13
1. Chandrasekhar, K., Kapoor, J. & Anishetty, S. A Prospective, Randomized Double-Blind, Placebo-Controlled Study of Safety and Efficacy of a High-Concentration Full-Spectrum Extract of Ashwagandha Root in Reducing Stress and Anxiety in Adults. Indian J. Psychol. Med. 34, 255–263 (2012).
2. Kulkarni, S. K. & Dhir, A. Withania somnifera: An Indian ginseng. Prog. Neuropsychopharmacol. Biol. Psychiatry 32, 1093–1105 (2008).
3. Mirjalili, M. H., Moyano, E., Bonfill, M., Cusido, R. M. & Palazón, J. Steroidal Lactones from Withania somnifera, an Ancient Plant for Novel Medicine. Molecules 14, 2373–2393 (2009).
4. Bhattacharya, S. K., Bhattacharya, A., Sairam, K. & Ghosaf, S. Anxiolytic-antidepressant activity of Withania somnifera glycowithanolides : an experimental study. Phytomedicine 7, 463–469 (2000).
5. Kumar, A. & Kalonia, H. Effect of Withania somnifera on Sleep-Wake Cycle in Sleep Disturbed Rats: Possible GABAergic Mechanism. Indian J Pharm Sci 70, 806–810 (2008).
6. Bhatnagar, M., Sharma, D. & Salvi, M. Neuroprotective Effects of Withania somnifera Dunal .: A Possible Mechanism. Neurochem Res 34, 1975–1983 (2009).
7. Naidu, P. S., Singh, A. & Kulkarni, S. K. Effect of Withania somnifera Root Extract on Reserpine-induced Orofacial Dyskinesia and Cognitive Dysfunction. Phytother. Res. 20, 140–146 (2006).
8. AK, T., S, D., RH, S. & PK, D. Alterations in the sensitivity of 5(th) receptor subtypes following chronic asvagandha treatment in rats. Anc Sci Life. 17, 169–81 (1998).
9. Grover, A., Shandilya, A., Agrawal, V., Bisaria, V. S. & Sundar, D. Computational Evidence to Inhibition of Human Acetyl Cholinesterase by Withanolide A for Alzheimer Treatment Computational Evidence to Inhibition of Human Acetyl Cholinesterase by Withanolide A for Alzheimer Treatment. 37–41
10. R, S. et al. Systemic administration of defined extracts from Withania somnifera (Indian Ginseng) and Shilajit differentially affects cholinergic but not glutamatergic and GABAergic markers in rat brain. Neurochem Int. 30, 181–90. (1997).
11. Mikolai, J. et al. In Vivo Effects of Ashwagandha ( Withania somnifera ) Extract on the Activation of Lymphocytes. J. Altern. Complement. Med. 15, 423–430 (2009).
12. Gupta, Y., Sharma, S., Rai, K. & Katiyar, C. Reversal of paclitaxel induced neutropenia by Withania somnifera in mice. Indian J Physiol Pharmacol. 45, 253–257 (2001).
13. Dar, N. J., Hamid, A. & Ahmad, M. Pharmacologic overview of Withania somnifera , the Indian Ginseng. Cell. Mol. Life Sci. 72, 4445–60 (2015).
14. Mohan, R. et al. Withaferin A is a potent inhibitor of angiogenesis. Angiogenesis 7, 115–122 (2004).
15. Durg, S., Dhadde, S. B., Vandal, R., Shivakumar, B. S. & Charan, C. S. Withania somnifera (Ashwagandha) in neurobehavioural disorders induced by brain oxidative stress in rodents: a systematic review and meta-analysis. J Pharm Pharmacol. 67, 879–99 (2015).
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