ASHWAGANDHA

The primary active component witherfarin A and similar compounds show wide ranging effects on cancers, metastasis and cancer stem cells that drive spread and resistance, but only in the lan. (see References) Direct clinical evidence has not been shown in cancer patients. Only one phase 2 trial in breast cancer patients has shown trends to increased survival, reported as not statistically significant ( see below ). The absorption and metabolism of ashwagandha extracts do not support their potential anti-cancer effects at present.

Some smaller trials do show positive results for improving metabolic health, in both glucose and cholesterol management. But the clearest evidence is for managment of stress, anxiety with possible benefits to sleep patterns, reducing treatment related fatigue.

A few trials have shown effects in increasing testosterone should be carefully considered or avoided for prostate cancers. But most importantly, these trials have also reported increases in circulating glutathione, an anti-oxidant associated with cancer progression.

TYPICAL ABSORPTION LEVELS

1 – 10%

EXAMPLES OF IMPROVED OUTCOMES

PENDING

PRE-DIAGNOSIS OR PREVENTION

Highlighted Studies

Eight patients had stage I, 33 stage II, 44 stage III, and 15 stage IV breast cancer. Fifteen patients were offered palliative chemotherapy and 85 were offered adjuvant chemotherapy. Patients in the group treated with W. somnifera root extract and chemotherapy had less fatigue than did those in the control group. QoL was significantly better than in the control group. There was no difference in the haematological parameters or 24-month overall survival for all stages [study 74% versu...

Numerous [laboratory] studies have shown the anti-cancer effect of Ashwagandha or its major component, WFA, in various cancers. Ashwagandha can be used as an adjunct therapy that can reduce the adverse effects of radio and chemotherapy due to its anti-inflammatory and antioxidant properties. Ashwagandha can also be combined with other conventional treatments such as chemotherapies to synergize and potentiate the effects of chemotherapy due to its ability to aid in chemosensitization. All evid...

WA holds immense potential as an anti-tumor agent, and its pharmacological properties have shown significant antitumor efficacy in various cancers. As research in this field continues to progress, we expect a better understanding of the precise mechanisms of WA’s action, its toxicity profile, and advancements in delivery strategies. These efforts will contribute to establishing WA as a potent and safe candidate for cancer treatment, opening new possibilities for clinical applications and im...

We found that Withaferin A induces the production of molecules from lung cancer cells that increase the infiltration of immune cells but are not able to kill cancer cells. Notably, in an immunocompetent mouse model of lung cancer, treatment with a combination of Withaferin A and an immunotherapy regimen showed more effectiveness than immunotherapy alone in activating immune cells and reducing tumor growth. This study presents a novel approach that can be tested clinically to improve lung canc...

TABLE OF REFERENCES

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URL	Category	Rating	Highlight	Highlight 2	Dose mg/kg
https://www.ejcancer.com/article/S0959-8049(12)00168-2/abstract	Lab study- adjunct	3.5	Fifteen patients were offered palliative chemotherapy and 85 were offered adjuvant chemotherapy. Patients in the group treated with W. somnifera root extract and chemotherapy had less fatigue than did those in the control group (PFS p<0.001 and SCFS p<0.003). QoL was significantly better (p=0.0001) than in the control group. There was no difference in the haematological parameters or 24-month overall survival for all stages [study 74% versus control 56% (p=0.174)]; however, there was a trend for longer survival in the patients treated with W. somnifera root extract plus chemotherapy.ime of analysis was 20 months, with a median overall survival rate of 26 months (range = 3-72 months) and 15 months, respectively, in the study and control arm patients. ..the 24-month overall survival was 72% versus 56% . The above results were not statistically significant (P = .176) but the trend of the plot was in favor of the study arm	In our study, we observed similar overall survival figures among WS-treated patients, though the trend is in favor of the study arm. The favorable trend may be by chance or difference in disease load or higher number of HER-2 positive patients in the control arm. In the study and control groups, we had the same number of stage III and IV patients (29 in each arm). More control than study group patients (25 vs 35) received the TAC regimen, which could have favored survival in the control arm. It is also possible that WS enhances the cytotoxicity of chemotherapy mediated through its induction of apoptosis or interference with the estrogen receptor	2mg x 3 daily
https://www.researchgate.net/publication/334541565_Identification_of_Withaferin_A_as_a_Potential_Candidate_for_Anti-Cancer_Therapy_in_Non-Small_Cell_Lung_Cancer	Lab study	3	First, we demonstrated that WA [Witherfarin A aka Ashwagandha] exhibited potent cytotoxicity in several lung cancer cells, as evidenced by low IC50 values. WA concurrently induced autophagy and apoptosis and the activation of reactive oxygen species (ROS), which plays an upstream role in mediating WA-elicited effects. The increase in p62 indicated that WA may modulate the autophagy flux followed by apoptosis	In vivo research also demonstrated the anti-tumor effect of WA treatment. We subsequently demonstrated that WA could inhibit the growth of lung CSCs [cancer stem cells], decrease side population cells, and inhibit lung cancer spheroid-forming capacity, at least through downregulation of mTOR/STAT3 signaling.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8960981/	Lab study	3	Withaferin-a, a steroidal lactone derived from the medicinal plant Withania somnifera Dunal (Solanaceae), has a wide range of pharmacological activities, including cardioprotective, anti-inflammatory, and anti-angiogenesis. It has been reported that withaferin-a induced cell apoptosis by inhibiting the expression or activation of STAT3 in ccRCC cells and other cancer cells.	The synergistic effect by combining our repurposed drugs with the clinically used first-line chemotherapy drugs (e.g., tyrosine kinase inhibitors, mTOR inhibitors and monoclonal antibodies against VEGF) is also worthwhile to investigate in the future work. Interestingly, the treatment effects of the combination of panobinostat with tyrosine inhibitor axitinib or proteasome inhibitor bortezomib have been demonstrated in vitro or in vivo ccRCC models.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5650357/	Lab study- adjunct	3	Withaferin A (WFA) alone or in combination with cisplatin (CIS) significantly inhibited the spheroid formation (tumorigenic potential) of isolated ALDH1 CSCs in vitro and significantly reduced its expression in tumors collected from mice bearing orthotopic ovarian tumor compared to control.	Treatment of animals with CIS alone significantly increased the ALDH1 CSC population in tumors, suggesting that CIS targets cancer cells but spares cancer stem cells, which undergo amplification. WFA and CIS combination suppresses the expression of securin an “oncogene”, suggesting that securin may serve as a downstream signaling gene to mediate the antitumor effects of WFA.	2
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4180068/	Lab study, Lab study- adjunct	3	The silent observation from this study is that treatment of mice bearing human ovarian tumors with CIS results in an unwanted expansion of cells that express CSC markers, what may lead to CIS resistance and recurrence of ovarian tumor. In contrast, WFA if employed alone or in combination with CIS ameliorates this unwanted effect. The data obtained from our study suggest that WFA alone or in combination with CIS may serve as a safer and more efficacious therapy for both first line and second line options for ovarian cancer. Go to:	These results suggest that combination of low dose of WFA (2 mg/kg) with suboptimal dose of CIS (6 mg/kg) is highly effective in suppressing tumor growth and metastasis of orthotopic ovarian tumors in nude mice. This indicates that it would be possible to reduce therapeutic dose of CIS when combined with WFA in humans to ameliorate side effects associated with high dosage of CIS.	2mg/kg
https://jcmtjournal.com/article/view/1266#sec13	Lab study	3	WA could efﬁ ciently block the formation of both CSCs and mCSCs in the UP-LN1 cell line, suggesting that WA may be considered an effective therapeutic agent for this type of GI malignancies.	Thus, the observation that WA treatment negatively regulated the CXCR4/CXCL12 chemotactic axis and molecules involved in IFN-γ-stimulated F cells, leading to making more CXCR4-positive mCSCs in cell numbers but not in increasing the number of CXCR4 sites on a per-cell basis, provides support for using WA as a potent anti-metastasis agent.	10mg/kg 3x week
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4924683/	Lab study- adjunct	3	We also found that WA is a potent small molecule that could override AKT-induced cell proliferation and tumor growth of colon cancer cells. Although we did not evaluate the metastasis of tumors overexpressing AKT due to the increase in tumor burden on animals, our results demonstrate that AKT represents an attractive target, and developing either pharmacological agents or derivatives of WA may be a viable therapeutic option for treating patients with metastatic colon cancer.	In our study, WA significantly inhibited phosphorylated-AKT (pAKT) without downregulating total AKT expression. Natural compounds, such as quercetin and brassinin, have been shown to inhibit AKT activity in many cancer cell types, including CRC [50], [51]. Earlier, we reported that WA downregulated AKT/NOTCH signaling and simultaneously induced apoptosis in a panel of colon cancer cell lines	5mg/kg
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5228601/	Lab study	3	Results of our current mouse experiments are consistent with in vitro data. The WS extract, administered orally, inhibited formation and growth of MDA-MB-231 cell xenografts in nude mice, indicating that the active ingredients of the WS extract are bioavailable after oral administration.[19] Six mice of the untreated group developed tumor metastasis to the lung, whereas none of the treated mice showed such tumor metastases	Furthermore, WS extract inhibited proliferation of xenografted MDA-MB-231 cells, reducing the size of xenografted tumors by 60% compared to the untreated control after 8 weeks of treatment (P < 0.05) [Figure 4]. In addition, after euthanasia, six of ten mice in the control group showed tumor metastasis to the lung, whereas none of the mice in WS-treated group developed metastasized tumor lesions in the lung	300
https://www.ajol.info/index.php/tjpr/article/view/119534/108992	Lab study	3	Withaferin A inhibits liver tumor invasion and angiogenesis by downregulation of cell signaling pathway leading to invasion and angiogenesis. It also inhibits tumor-associated macrophage infiltration leading to tumor inflammatory response. Therefore, withaferin A can be a promising candidate for the treatment of liver tumor invasion and angiogenesis.	A decrease in incidence of intrahepatic metastasis was observed from 90 % (9 of 10) to 10 % after withaferin A treatment. There was also suppression in lung metastasis on treatment with withaferin A. Incidence of lung metastasis in mice decreased from 80 (8 of 10) to 10 % (1 of 10).	3 and 5mg/kg
https://www.sciencedirect.com/science/article/pii/S1476558617301367#f0005	Lab study	3	Pathological analysis showed the complete absence of metastatic lesions in organs from WA-treated mice, whereas discrete metastasis to the lungs was observed in control tumors. Immunohistochemical analysis revealed the down-regulation of pAKT expression and epithelial-to-mesenchymal transition markers, such as β-catenin and N-cadherin, in WA-treated tumors in comparison to controls.	The dietary phytonutrient WA exhibited potent chemopreventive activity in the treatment of a mouse prostate cancer model harboring Pten deletions. A delay of prostate tumor progression was demonstrated to occur via the inhibition of the PI3K/AKT pathway by WA. The AKT-regulated proapoptotic proteins Par-4 and FOXO3A were up-regulated in Pten-KO mice treated with WA. Our findings suggest that WA may have clinical therapeutic benefits for prostate cancer patients harboring AKT-activating mutations, such as PTEN deletion.
https://onlinelibrary.wiley.com/doi/full/10.1111/cas.13266	Lab study- adjunct	3	Glucose metabolism-targeting therapeutic agents have effective antitumor activity against the CD133low cell population; the CSC-targeting agent, WFA, has effective antitumor activity against the CD133high cell population, as summarized in Figure 5(e). Although these glucose-targeting therapeutic agents and WFA are not available in a clinical setting at present, they are potent agents for overcoming gefitinib-induced DTPs and are worth evaluating in prospective clinical trials. The combination of these agents and gefitinib will be a promising therapeutic strategy to overcome EGFR-TKI resistance.	In order to overcome this treatment limitation, novel therapeutic strategies to eliminate CSCs have been developed.49-51 Withaferin A, a bioactive compound isolated from the plant Withania somnifera, is a potent inhibitor of CSCs.29 To the best of our knowledge, we are the first to show that WFA has a promising antitumor effect on lung cancer cells both in vitro and in vivo, and that WFA is a potent therapeutic agent to overcome gefitinib-induced DTPs	3mg 3 week
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8413038/	Lab study	3	To follow the prolonged therapeutic effect of WFA, these experimental mice were left untreated for ten additional days. It appeared that the developed immune response following WFA treatment maintained the reduced tumor growth (Figure 2(b)). These observations indicate that the WFA induces NK cell activation, thereby augmenting antitumor immunity to inhibit the development and progression of prostate tumors	The role of WFA is appreciated to polarize tumor-suppressive Th1-type immune response inducing natural killer cell activity and may provide an opportunity to manipulate the tumor microenvironment at an early stage to inhibit tumor progression. This article signifies the cumulative information about the role of WFA in modulating antitumor immunity and its potential in targeting prostate cancer.	8mg/kg
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4924683/	Lab study	3	In our study, WA significantly inhibited phosphorylated-AKT (pAKT) without downregulating total AKT expression. Natural compounds, such as quercetin and brassinin, have been shown to inhibit AKT activity in many cancer cell types, including CRC [50], [51]. Earlier, we reported that WA downregulated AKT/NOTCH signaling and simultaneously induced apoptosis in a panel of colon cancer cell lines [40]. Our current docking studies suggest that in AKT/HCT-116 cells, WA binds to AKT and inhibits the phosphorylation of AKT, resulting in the inhibition of many phenotypic cascades, such as cell proliferation, invasion, migration and tumor growth.	We also found that WA is a potent small molecule that could override AKT-induced cell proliferation and tumor growth of colon cancer cells. Although we did not evaluate the metastasis of tumors overexpressing AKT due to the increase in tumor burden on animals, our results demonstrate that AKT represents an attractive target, and developing either pharmacological agents or derivatives of WA may be a viable therapeutic option for treating patients with metastatic colon cancer.	5mg/kg
https://kd.nsfc.gov.cn/paperDownload/1000013978161.pdf	Lab study, Lab study- adjunct	3	In summary, the data of our preclinical study suggest that WA acts highly synergistically with oxaliplatin against Pancreatic cancer cells in vitro and in tumor xenograft models through ROS-mediated mitochondrial dysfunction and inhibition of PI3K/AKT signaling. Therefore, combination therapy of oxaliplatin and WA could become a novel approach for PC treatment. Clinical trials must be exploited to support this strategy for PC treatment	Consistent with tumor volumes, mean tumor weights were decreased dramatically in the combination group compared with other groups (Fig. 6B). Mice receiving oxaliplatin appeared to be sick with loss of appetite and weight loss, but no significant addition of toxicity in terms of progressive weight loss was observed in the combination group
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562581/	Lab study	2.5	We now demonstrate, for the first time, that WA exhibits significant activity against human breast cancer cells in culture and in vivo. The WA treatment decreased viability of MCF-7 (estrogen-responsive) and MDA-MB-231 (estrogen-independent) human breast cancer cells in a concentration-dependent manner. The WA-mediated suppression of breast cancer cell viability correlated with apoptosis induction characterized by DNA condensation, cytoplasmic histone-associated DNA fragmentation, and cleavage of poly-(ADP-ribose)-polymerase	The tumors from WA-treated mice exhibited reduced cell proliferation and increased apoptosis compared with tumors from control mice. These results point towards an important role of FOXO3a and Bim in regulation of WA-mediated apoptosis in human breast cancer cells.	4
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6314334/	Lab study	2.5	Oral WA administration (4 and 3 mg/kg) inhibited tumor initiation and progression of intestinal polyps formation in APCMin/+ mice and colon carcinogenesis in the AOM/DSS mouse model. WA-administered mice showed a significant reduction in both number duodenum, 33%; jejunum, 32%; ileum, 43% and colon 59% and size of polyps in APCMin/+ mice compared with the respective controls.	Molecular studies suggested that WA inhibited the expression of inflammatory (interluekin-6, tumor necrosis factor-alpha and cyclooxygenase-2), pro-survival (pAKT, Notch1 and NF-κB) markers in APCMin/+ and AOM/DSS models. The results suggest that WA is a potent agent for preventing colon carcinogenesis and further investigation is required to show clinical utility of the agent.	3 , 4mg/kg
https://onlinelibrary.wiley.com/doi/10.1002/ijc.25938	Lab study	2.5	On the basis of the data presented here, we conclude that WFA is a potent breast cancer anti-metastatic agent where its activity, at least in part, is mediated through its effects on vimentin and vimentin ser56 phosphorylation. As it is a natural compound that possesses minimal toxicity, we predict that WFA can be taken for long durations and at low doses, perhaps in the preventative setting	Higher doses of WFA at 4 mg/kg inhibited both metastasis and tumor growth. Tumor growth inhibition at this dose is consistent with a previous report showing a role of FOXO3A and Bim in the regulation of WFA-mediated apoptosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4009451/	Lab study	2.5	We uncovered a novel mechanism by which withaferin A inhibits growth of breast cancer cells in vitro and in vivo, which involves activation of RSK and ERK. We also demonstrate a feed-forward loop of ERK and RSK that results in concurrent activation of CHOP and pElk1, their recruitment to DR5 promoter leading to DR5 activation. Our results thus demonstrate the integral role of a previously unrecognized functional crosstalk between withaferin A and ERK/RSK and CHOP/Elk1 axes in breast tumor growth inhibition	Here, we show that WFA is more effective than three other known DR5 activators, TRAIL, etoposide and celecoxib, in activation of DR5 in breast cancer cells hence, appears to be a good candidate for further development as an effective DR5 inducer
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5033248/	Lab study- adjunct	2	we conclude that combining a small dose of DOXIL with suboptimal dose of WFA is highly effective in targeting CSCs, which may lead to reduction in development of drug resistance and recurrence of ovarian cancer. Application of a small dose of DOXIL in combination with suboptimal dose of WFA is expected to reduce unwanted side effects caused by high doses of DOXIL used	There has been an increasing support for natural compounds when developing new treatments for cancer to enhance the therapeutic effect of an anti-neoplastic agent. This allows a lower dose to be used while achieving the same anti-neoplastic effect and reducing the side effects. WFA is a bioactive, cell permeable compound isolated from the plant Withania somnifera is an anticancer and anti-inflammatory compound and possesses cardio-protective properties [36–40]. In our previous studies, we showed that WFA when combined with doxorubicin elicits synergistic effects on inhibition of cell proliferation of ovarian cancer cells	2
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4622669/	Lab study	1.5	WA inhibits the growth and survival of DLBCL by interacting and inhibiting the activity of the chaperone Hsp90, resulting in reduced expression of its client proteins.15 Studies also indicate that WA has no noticeable toxicity on normal lymphocytes28, and our results illustrate that WA does not appear to affect proliferating colon epithelial cells in vivo. Further analyses on in vivo stability of WA and its effects on normal tissues need to be completed in order evaluate the clinical potential of WA as a therapeutic for DLBCL but current findings are promising.	We suggest that the reduced protein levels of Akt are a result of decreased Hsp90 function as Akt is a confirmed client protein of the Hsp90/cdc37 chaperone complex.43,44 Some therapeutics have targeted the PIP3/AKT cascade due to the constitutive activation of the pathway in a variety of cancers.Further analyses on in vivo stability of WA and its effects on normal tissues need to be completed in order evaluate the clinical potential of WA as a therapeutic for DLBCL but current findings are promising.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7125369/	Absorption and dosage, Human study	N/A	This makes WA is an attractive compound for chemosensitization and to elicit cell death in chemoresistant cell types. Thus WA can synergize with other anticancer agents and its P-glycoprotein modulating activity can be exploited for improving the oral bioavailability and intratumoral concentrations of co-administered anticancer drugs [27]. Further clinical studies of WA as an adjunctive to chemotherapy in osteosarcoma are warranted. There is also preliminary evidence related to the activity of WA in gastric, thyroid and ovarian cancer. Here again, the utility of WA as an adjunctive treatment to standard modalities could be evaluated.	The corresponding Human Equivalent Dose (HED) is approximately 325 mg/kg/day. A safety factor of five was applied to obtain the Maximum Recommended Starting Dose (MRSD) of 65 mg/kg/day of the formula in humans [17]. Considering the average human weight to be 60 kg we arrived at an MRSD of 3900 mg/day. In the present study the starting dose of W. somnifera extract used is 1600 mg, which was gradually escalated to 4800 mg/day.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6862083/	Absorption and dosage	N/A	As reviewed herein, the recent clinical trials using randomized double-blind placebo control designs using WS extracts have shown that at specified dosage ranging from 200 mg/kg to 1000 mg/kg WS was not only effective, but most importantly at these dosages WS was safe and well tolerated. Further, numerous studies have shown anti-cancer efficacy using either WS or its major component WFA in human cancer cells lines and in murine models	First, given the safety record of WS, it can be used as an adjunct therapy that can aid in reducing the adverse effects associated with radio and chemotherapy due to its anti-inflammatory properties. Second, WS can also be combined with other conventional therapies such as chemotherapies to synergize and potentiate the effects due to radiotherapy and chemotherapy due to its ability to aid in radio- and chemosensitization, respectively
https://www.frontiersin.org/articles/10.3389/fphar.2022.975320/full#h3	Absorption and dosage	N/A	Another study by Dai et al. (2019) assessed oral bioavailability in male rats by administering Withaferin A as 5 mg/kg intravenously and 10 mg/kg orally (Dai et al., 2019). Results for oral bioavailability were 32.4 ± 4.8%, depicting low systemic absorption of the compound (Dai et al., 2019). The same study also conducted an in vitro analysis which revealed rapid depletion with half-life of 5.6 min of Withaferin A in liver microsomes; furthermore, the study verified first-pass metabolism by revealing 21% remaining Withaferin A over 1 h time period	Among the seven constituents evaluated, only three, Withaferin A, Withanoside IV, and 1,2-deoxywithanstramonolide, were found to have increased oral absorption from the stomach lining, lower half-life, and lower oral clearance (Modi et al., 2022). Furthermore, Withaferin A and 1,2-deoxywithastramonolide constituents were detectable in plasma up till 10 h which depicted possibility of lower elimination rate for these constituents (Modi et al., 2022).
https://analyticalsciencejournals.onlinelibrary.wiley.com/doi/10.1002/bmc.4573	Absorption and dosage	N/A	The developed and validated analytical methods were successfully applied to the pharmacokinetic studies and in vitro measurement of WA. The oral bioavailability was determined to be 32.4 ± 4.8% based on intravenous (5 mg/kg) and oral (10 mg/kg) administrations of WA in male rats	Stability of WA was similar between male rat and human in simulated gastric fluid (stable), in intestinal microflora solution (slow decrease) and in liver microsomes (rapid depletion, with a half-life of 5.6 min). As such, the first-pass metabolism of WA was further verified by rat intestine-liver in situ perfusion, revealing that WA rapidly decreased and 27.1% remained within 1 h
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0275432#sec020	Absorption and dosage	N/A	ADMET analysis of Ashwagandhanolide inferred that the compound was hydrophobic with moderate intestinal permeability, good intestinal absorption, poor skin permeability and relatively low VDss value (-1.652) indicating that the compound did not easily cross the blood-brain barrier (BBB). The Conceptual DFT study performed through the analysis of the chemical ractivity descriptors revealed the favorable characteristics of this compound for its consideration as a good therapeutic drug.	The drug’s absorption from an orally administered solution is predicted by the intestinal absorption (human) value. This value for Ashwagandhanolide is greater than 60%, indicating good absorption.
https://www.researchgate.net/publication/235733546_Phytochemical_variability_in_commercial_herbal_products_and_preparations_of_Withania_somnifera_Ashwagandha	Absorption and dosage	N/A	The results clearly suggest that the commercial products vary by several orders of magnitude with respect to their phytochemical composition. Since phytochemicals, particularly unique ones (like withanolides in Ashwagandha) are raison d’etre for health benefits of the herbs, inordinate variations in their daily dose may reverberate in blotchy health benefit(s)	The results revealed wide variations in the content of all seven constituents tested. More than 70-fold variation in the daily intake of withaferin A (the main active constituent of Ashwa-gandha) was found in the products. The study thus emphasizes the need for stringent phytochemical stand-ardization of herbal products.
https://examine.com/supplements/ashwagandha/research/	Absorption and dosage	N/A	There has been reported to be high variability in the amount of active withanolides in common nutritional supplements,[31] which may be due either to lack of standardization of root powder. Unless otherwise standardized to a certain percentage, the amount of active Withanolide A (seen as the primary ingredient) and Withaferin-A are 1% of dry weight of the leaves (with negligible content in the roots) of Withania Somnifera.[32]	Studies on ashwagandha have used daily dosages ranging from 120–5,000 mg of a root extract. The most common dosing protocol is 600 mg daily, divided into two doses, with one taken in the morning with breakfast and the other in the evening. Note that while studies may use standardized extracts or proprietary formulas, variations in extraction methods, formulation, or composition can affect physiological response.	Withaferin A[11] (22.31+/-1mg/g dry weight of leaves and 0.92+/-0.4mg/g in roots