Scientific Name Withania somnifera (synonym: Physalis somnifera) Family Solanaceae Other Common Names : Ajagandha, Amangura, Amukkirag, Asan, Asana, Asgand, Asgandh, Asgandha, Ashagandha, Ashvagandha, Ashwaganda, Ashwanga, Asoda, Asundha, Caution
Ashwagandha should not be confused with Physalis alkekengi, both plants are commonly known as Winter Cherry. Also, avoid confusion with other herbs used as adaptogens, such as American Ginseng, Panax Ginseng, and Eleuthero.
Ashwagandha is a small evergreen shrub found in dry areas of India and the Middle East, as well as parts of Africa (14863, 32533). Ashwagandha is used in traditional medicine, usually as an adaptogenic herb (14863, 32525, 90650, 90651). Adaptogens are theorized to help the body resist physiological and psychological stress.
Ashwagandha is sometimes substituted or adulterated with a similar plant, Withania coagulans (3710).
Coronavirus disease 2019 (COVID-19): Despite claims to the contrary, there is no good evidence to support using ashwagandha for COVID-19. Recommend healthy lifestyle choices and proven prevention methods inst
ead.
Possibly Safe when used orally and appropriately, short-term. Ashwagandha has been used with apparent safety in doses of up to 1250 mg daily for up to 6 months (3710, 11301, 19271, 90649, 90652, 90653, 97292, 101816, 102682, 102683) (102684, 102685, 102687, 103476, 105824, 109586, 109588, 109589, 109590, 116648). ...when used topically. Ashwagandha lotion has been used with apparent safety in concentrations up to 8% for up to 2 months (111538).
PREGNANCY: Likely Unsafe when used orally. Ashwagandha has abortifacient effects (12).
LACTATION: Insufficient reliable information available; avoid using.
Orally, ashwagandha seems to be well-tolerated. Topically, no adverse effects have been reported. However, a thorough evaluation of safety outcomes has not been conducted.
Orally: Diarrhea, gastrointestinal upset, nausea, and vomiting. However, these adverse effects do not commonly occur with typical doses.
Orally: Some case reports raise concerns about acute hepatitis, acute liver failure, hepatic encephalopathy, the need for liver transplantation, and death due to liver failure with ashwagandha treatment.
Anxiety. Small clinical studies suggest that oral ashwagandha might reduce anxiety.
Oral ashwagandha may modestly improve symptoms of anxiety in patients with GAD.
Oral ashwagandha may modestly improve sleep in patients with insomnia or non-restorative sleep.
Oral ashwagandha seems to help reduce stress and may also reduce stress-related weight gain.
Insufficient Reliable Evidence to Rate
A small clinical study suggests that oral ashwagandha may modestly improve well-being, sleep, and alertness in elderly patients.
It is unclear if topical ashwagandha is beneficial for androgenic alopecia.
It is unclear if ashwagandha is beneficial for attenuating the metabolic side effects of antipsychotic agents.
Although there has been interest in using oral ashwagandha for asthma, there is insufficient reliable information about the clinical effects of ashwagandha for this condition.
It is unclear if ashwagandha is beneficial for improving athletic performance.
Oral ashwagandha has only been evaluated in combination with other ingredients; its effect when used alone is unclear.
Oral ashwagandha has only been evaluated in combination with other ingredients; its effect when used alone is unclear.
It is unclear if oral ashwagandha is beneficial for improving cognitive function in adults with bipolar disorder.
Although there has been interest in using oral ashwagandha for bronchitis, there is insufficient reliable information about the clinical effects of ashwagandha for this condition.
It is unclear if oral ashwagandha is beneficial for improving balance in patients with cerebellar ataxia.
Evidence is limited to one small clinical study in patients with breast cancer.
It is unclear if oral ashwagandha is beneficial in patients with COPD.
Although there has been interest in using oral ashwagandha for cognitive function, there is insufficient reliable information about the clinical effects of ashwagandha for this condition.
It is unclear if oral ashwagandha is beneficial in patients with cognitive impairment.
Oral ashwagandha has only been evaluated in combination with other ingredients; its effect when used alone is unclear.
Oral ashwagandha has only been evaluated in combination with other ingredients; its effect when used alone is unclear.
It is unclear if oral ashwagandha is beneficial for depression.
It is unclear if oral ashwagandha is beneficial for type 2 diabetes.
It is unclear if oral ashwagandha is beneficial for fatigue.
Although there has been interest in using oral ashwagandha for fibromyalgia, there is insufficient reliable information about the clinical effects of ashwagandha for this condition.
Although there has been interest in using oral ashwagandha for hiccups, there is insufficient reliable information about the clinical effects of ashwagandha for this condition.
It is unclear if ashwagandha is beneficial for hypercholesterolemia.
It is unclear if ashwagandha is beneficial for hypothyroidism.
Although there has been interest in using oral ashwagandha for infertility in females, there is insufficient reliable information about the clinical effects of ashwagandha for this condition.
It is unclear if topical ashwagandha is beneficial for oral lichen planus.
It is unclear if oral ashwagandha is beneficial for male infertility.
Oral ashwagandha may be beneficial for menopausal symptoms.
It is unclear if ashwagandha is beneficial for OCD.
Oral ashwagandha has only been evaluated in combination with other ingredients; its effect when used alone is unclear.
Oral ashwagandha has only been evaluated in combination with other ingredients; its effect when used alone is unclear.
It is unclear if oral ashwagandha is beneficial for improving psychological well-being in college students.
It is unclear if oral ashwagandha is beneficial for improving symptoms of RA.
Small clinical studies suggest that oral ashwagandha root extract may help improve sexual arousal and sexual desire in some females and males with sexual dysfunction.
Oral ashwagandha has only been evaluated for smoking cessation in combination with other ingredients; its effect when used alone is unclear.
Although there has been interest in using oral ashwagandha for tuberculosis, there is insufficient reliable information about the clinical effects of ashwagandha for this condition.
Although there has been interest in using oral ashwagandha for vitiligo, there is insufficient reliable information about the clinical effects of ashwagandha for this condition.
Although there has been interest in using topical ashwagandha for healing of skin ulcers and skin sores, there is insufficient reliable information about the clinical effects of ashwagandha for this condition.
It is unclear if topical ashwagandha is beneficial in individuals with wrinkled skin. More evidence is needed to rate ashwagandha for these uses.
Ashwagandha has most often been used in doses of up to 1000 mg daily for up to 12 weeks. See Effectiveness section for condition-specific information.
Ashwagandha extract is often standardized to withanolide content, with concentrations ranging from 1.5% to 35% (19271, 90650, 90652, 90653, 106786).
Research is limited; typical dosing is unavailable.
Ashwagandha root by Swiss Herbals, used in some clinical trials, has been standardized to 1.5% withanolides (19271). Another standardized product is Sensoril (Natreon, Inc.), containing a minimum of 8% withanolides and 32% oligosaccharides, and a maximum of 2% withferin A (90653). KSM-66 (Ixoreal Biomed) is standardized to withanolide ≥ 5% and contains alkaloids, the amino acids threonine, valine, methionine, isoleucine, lysine, aspartic acid, and arginine, complex sugars such as oligosaccharides and fructooligosaccharides, and vitamin A, calcium, and iron (90650, 90652, 109586). Shoden (Arjuna Natural Inc) is standardized to 35% withanolide glycosides (101816, 103476, 106786).
Interaction Rating Moderate Be cautious with this combination. Severity HIGH Occurrence POSSIBLE Level of Evidence B (Clinical cohort study)
Theoretically, taking ashwagandha with antidiabetes drugs might increase the risk of hypoglycemia.
Interaction Rating Moderate Be cautious with this combination. Severity MODERATE Occurrence POSSIBLE Level of Evidence D (In vitro or animal study) Theoretically, taking ashwagandha wth antihypertensive drugs might increase the risk of hypotension.
Interaction Rating Moderate Be cautious with this combination. Severity HIGH Occurrence POSSIBLE Level of Evidence D (Theoretical based on pharmacology)
Theoretically, taking ashwagandha might increase the sedative effects of benzodiazepines.
Interaction Rating Moderate Be cautious with this combination. Severity HIGH Occurrence POSSIBLE Level of Evidence D (Theoretical based on pharmacology)
Theoretically, taking ashwagandha might increase the sedative effects of CNS depressants.
Interaction Rating Minor Be watchful with this combination. Severity MILD Occurrence POSSIBLE Level of Evidence D (In vitro or animal study)
Theoretically, ashwagandha might decrease the levels and clinical effects of CYP1A2 substrates.
Interaction Rating Minor Be watchful with this combination. Severity MILD Occurrence POSSIBLE Level of Evidence D (In vitro or animal study)
Theoretically, ashwagandha might decrease the levels and clinical effects of CYP3A4 substrates.
Interaction Rating Moderate Be cautious with this combination. Severity HIGH Occurrence POSSIBLE Level of Evidence D (Theoretical based on pharmacology) Theoretically, taking ashwagandha with hepatotoxic drugs might increase the risk of liver damage.
Interaction Rating Moderate Be cautious with this combination. Severity HIGH Occurrence POSSIBLE Level of Evidence D (In vitro or animal study) Theoretically, taking ashwagandha might decrease the effects of immunosuppressants.
Interaction Rating Moderate Be cautious with this combination. Severity MODERATE Occurrence PROBABLE Level of Evidence B (Lower quality RCT) Ashwagandha might increase the effects and adverse effects of thyroid hormone.
Theoretically, taking ashwagandha with hepatotoxic supplements might increase the risk of liver damage.
Theoretically, ashwagandha might have hypotensive effects.
Theoretically, ashwagandha might have sedative effects.
There is insufficient reliable information available about the presentation or treatment of overdose with ashwagandha.
Following oral intake of ashwagandha 400-500 mg in healthy adults, ashwagandha constituents withanoside IV, withanolide A, withaferin A, and 12-deoxy-withastramonolide are quickly absorbed and reach peak plasma concentrations within 0.9-1.6 hours (113612, 116647). Peak concentrations of these constituents, following intake of ashwagandha 500 mg, range from 0.6 to 5.5 ng/mL and are quantifiable in plasma for up to 12 hours (113612). After a single 400 mg dose, peak plasma concentrations of constituents ranged from 0.4 to 4.7 ng/mL in males and 0.6 to 3.2 ng/mL in females (116647).
The concentration of withanolides is greater than that of withanosides in plasma. Gut glucosidase may hydrolyze withanosides, resulting in the bioactive constituent sominone 2 to 12 hours after oral administration of ashwagandha 500 mg (113612). After a single 400 mg dose of ashwagandha in healthy adults, half-lives of constituents ranged from 2.5-5 hours in males and 1.6-4.3 hours in females (116647).
The applicable parts of ashwagandha are the root and berry. Ashwagandha contains several active constituents including alkaloids (isopelletierine, anaferine), steroidal lactones (withanolides, withaferins), and saponins (4116, 11301). It also contains salvigenin, withaperuvin 1, eucommiol, vicosalactone B, anamides D and E, and asomidienone (108744). Ashwagandha does not contain nicotine as some researchers have reported (3710). Some of the withanolides are structurally similar to ginsenosides from ginseng (14863). Withaferin A has a similar structure to digoxin, and can be bound and neutralized by digoxin immune fab (Digibind) (14863).
Ashwagandha does not seem to have any effect on the laboratory monitoring of acetaminophen, salicylates, phenytoin, phenobarbital, carbamazepine, valproic acid, procainamide (including N-acetyl procainamide), theophylline, gentamicin, or tobramycin (14863).
Animal model research suggests that ashwagandha has a variety of pharmacological effects including analgesic effects (3710).
In animal research, ashwagandha had anti-inflammatory effects in the bladder (3711).
Some researchers think ashwagandha has a so-called "anti-stressor" effect (4113). Preliminary research suggests ashwagandha suppresses stress-induced increases of dopamine receptors in the corpus striatum of the brain (3710). It also appears to reduce stress-induced increases of plasma corticosterone, blood urea nitrogen, and blood lactic acid (11301). Preliminary clinical research in adults with general anxiety disorder shows that taking ashwagandha, standardized to 35% withanolides, 60-120 mg orally daily for 60 days improves cortisol levels when compared with placebo (114792). Other preliminary research in healthy adults shows that taking liposomal ashwagandha 225 mg orally daily modestly improves fatigue scores, but not total mood scores when compared with placebo (114786).
Ashwagandha is of interest for the treatment of cancer. In laboratory research, the withanolides and ashwagandha extract had cytotoxic effects in cancer cells and other laboratory models (32509, 32517, 32518, 32538, 32548, 32551, 32552).
Ashwagandha might have anticonvulsant activity, by binding to the gamma-aminobutyric acid (GABA) receptor (3710).
Human research shows that ashwagandha increases serum serotonin levels and morning salivary cortisol levels, suggesting that the antidepressive and anxiolytic effects are related to the hypothalamus, anterior pituitary gland, and adrenal (HPA) axis (113608, 113609).
Ashwagandha is of interest for diabetes. In humans and in animal diabetic models, ashwagandha extract reduces blood glucose and glycated hemoglobin (HbA1c). In vitro, ashwagandha extract increases the uptake of glucose into adipocytes and muscle cells. Possible active constituents include withaferin A and withanolide A. In addition, three withanolides inhibited alpha-glucosidase in vitro (102685).
Animal model research suggests that ashwagandha has a variety of pharmacological effects including antioxidant effects (4116, 11301, 32558, 102685).
Animal model research suggests that ashwagandha has a variety of pharmacological effects including analgesic and antipyretic effects (3710).
Ashwagandha seems to have anxiolytic effects in laboratory research (32506), possibly by acting as a gamma-aminobutyric acid (GABA) mimetic agent (3710). Animal studies have demonstrated that ashwagandha can enhance serotonergic transmission through modulation of the postsynaptic serotonin (5-HT) receptors (95618).
In animal experiments, ashwagandha decreased blood pressure (32560).
Ashwagandha and its constituents seem to have immunomodulatory effects. The withanolides and sitoindosides seem to cause a mobilization of macrophages, phagocytosis, and lysosomal enzymes (11301). In healthy adults, an ethanolic extract of ashwagandha root and leaf has been shown to increase production of immunoglobulins, interferon-gamma, interleukin-4, and T cells, B cells, and natural killer cells when compared with baseline (106786). Animal research also suggests ashwagandha might reduce cyclophosphamide-induced immunosuppression and leukopenia (3711, 4114, 32550). Ashwagandha also seems to increase bone marrow cell and white blood cell count in radiation-treated animals (3711). It remains unclear, however, what net effect whole ashwagandha preparations have on the immune system (3710, 3711).
In vitro studies using human liver microsomes show that the water, ethanol, methanol, and ethyl acetate extracts of ashwagandha root may induce cytochrome P450 (CYP) 3A4 enzymes, although any clinical significance is unclear. The ethanol and methanol extracts may also inhibit CYP2B6 (108744).
In animal and human research, ashwagandha or its constituents improved memory function (32563, 90653). Mechanisms of action may involve the restoration of pre- and post-synapses in cortical neuron axons and dendrites, increased axonal density, or increased peripheral nervous system myelin (32526). Also, the withanolides have shown cholinesterase inhibitory potential in laboratory research (32521, 32522). Preliminary clinical research in healthy adults shows that taking liposomal ashwagandha 225 mg orally daily modestly improves performance on some, but not all, memory function tests when compared with placebo (114786).
Ashwagandha is thought to have neuroprotective and adaptogenic effects. In an animal model of alcohol addiction, ashwagandha reduces alcohol intake and withdrawal anxiety. The mechanism of action may be related to increased serotonin or gamma-aminobutyric acid levels but not alterations in cortico hippocampal dopamine (112629).
In clinical research, ashwagandha seems to improve sperm count and motility in adult males. These effects seem to be related to improved levels of testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin (19275). Preliminary clinical research in adults with general anxiety disorder shows that taking ashwagandha, standardized to 35% withanolides, 60-120 mg orally daily for 60 days improves testosterone levels when compared with placebo (114792).
Ashwagandha seems to stimulate respiratory function (3710).
Central nervous system depressant properties have been reported in animal studies (11301).
Ashwagandha seems to cause smooth muscle relaxation (3710).
Ashwagandha seems to stimulate thyroid synthesis and/or secretion (3710). In clinical and animal research, ashwagandha has been reported to stimulate thyroid function, increasing serum triiodothyronine (T3) and thyroxine (T4) concentrations and reducing serum thyroid stimulating hormone (TSH) levels (19281, 19282, 97292).
Adaptogens, Cytochrome P450 1A2 (CYP1A2) Inducers, Cytochrome P450 3A4 (CYP3A4) Inducers, Hepatotoxic Agents, Hypoglycemic Agents, Immunomodulators, Immunostimulants, Sedative-Hypnotic Agents, Testosterone Enhancers
Literature Review Current Through: 2/13/2026, Last Updated: 7/5/2026
The contents of this resource are not intended to be a substitute for professional medical advice, diagnosis, or treatment. Clinical input is needed from a qualified healthcare provider before taking any supplement or starting any therapy. Do not delay or disregard seeking medical advice or treatment based on any information displayed in this resource.
We use cookies to analyze website traffic and optimize your website experience. By accepting our use of cookies, your data will be aggregated with all other user data.