Despite widescale use, ashwagandha is considered generally safe and without major adverse effects. In clinical trials, there have been no reports of serum liver enzyme elevations occurring during therapy and no mention of serious adverse events or hepatotoxicity.
Ashwagandha, despite being widely used and generally considered safe with no major adverse effects in clinical trials, has been associated with rare cases of clinically apparent liver injury. These cases typically presented 2 to 12 weeks after starting ashwagandha, showing symptoms like cholestatic or mixed pattern of injury, jaundice, and pruritus. Notably, there were no prominent immunoallergic or autoimmune features observed. Although jaundice could be prolonged, it ultimately resolved without fatalities or chronic damage. The reported liver injuries were linked to commercial herbal products labelled to contain ashwagandha. While some cases were attributed to ashwagandha itself or its components, others raised concerns about contaminants in herbal preparations due to mislabeling or unknown ingredients. Despite these rare occurrences, clinically apparent liver injury from ashwagandha is infrequent (LiverTox, 2019).
Likelihood score: C (probable cause of clinically apparent liver injury).
Mechanism of Injury
The cause of hepatotoxicity from products containing ashwagandha is unclear. The possibility of mislabeling or adulteration with hepatotoxic herbal products is frequently an issue in commercial multi-ingredient dietary supplements (LiverTox, 2019).
Outcome and Management
The few cases of ashwagandha associated liver injury have been mild-to-moderate in severity and self-limited in course without acute liver failure or persistent liver injury. In most instances, the liver injury subsides within 1 to 3 months of discontinuing the herbal product. Rechallenge with the same product should be avoided (LiverTox, 2019).
Withania TGA Warning
The Australian regulator of medicine, the TGA, has issued a safety alert concerning Withania somnifera (dated 22 February 2024)
Medicines and herbal supplements containing the herb Withania somnifera may cause serious side effects (known as ‘adverse events’) in some people.
Withania should not be prescribed to people who have or have had liver disease.
Key messages from the alert:
Symptoms of liver disease include:
- yellowing of the skin or eyes
- dark urine
- nausea
- vomiting
- unusual tiredness
- weakness
- stomach or abdominal painÂ
- loss of appetite.
- The TGA is monitoring reports of gastrointestinal side effects experienced by consumers taking products containing Withania somnifera, such as sudden severe nausea, vomiting and diarrhoea.
- In some reports, vomiting and diarrhoea occurred after a single dose.
The TGA mentions reactions resolved after discontinuation of the product, but 16 cases were still severe enough to require hospitalisation.
Some of these cases involved other ingredients known to cause gastrointestinal side effects, but severe reactions requiring hospitalisation are not expected from these ingredients. However, it is still possible they may have contributed in some cases.
The TGA also mentions that they have received 12 reports of “liver problems†experienced by consumers taking products containing Withania somnifera up to 5 February 2024. These may be the 12 published cases reviewed below although the TGA later refers to further cases overseas.
Seven of the TGA reports had enough information to suggest a liver injury that may have been caused by Withania somnifera. In 4 of these cases there were no other ingredients likely to have contributed to the liver injury. The other 3 cases involved additional products or ingredients that may have contributed to liver injury. Most patients recovered after they stopped using Withania somnifera, although some required medical treatment. Four cases required hospitalisation.
In addition to these reports, there have also been further overseas reports in the scientific literature and multiple cases reported to regulators in other countries that suggest Withania somnifera may cause liver injury.Â
TGA Database of Adverse Event Notifications (DAEN)
A search of DAEN lists 271 reports (cases) involving withania having been reported to the TGA (as of 23rd February 2024). 242 involved a single suspected medicine. No death reported. The majority of the symptoms were gastrointestinal complaint, hypersensititivity, rash, headache, malaise, dizziness, paraesthesia and fatigue. A report from July 2023 included reaction terms such as crying, depressed mood, and suicidal ideation which are all very unlikely to be associated with use of withania.
TGA advice to health professonals
Health professionals should be aware that products containing Withania somnifera can cause acute, severe vomiting and diarrhoea that may be mistaken for infectious gastroenteritis.Â
In very rare cases, these products may also case liver injury in some individuals. When treating patients who are presenting with symptoms of liver injury, practitioners should consider whether a complementary medicine could be involved. Use of medicines or herbal supplements containing Withania somnifera should be avoided in patients with existing or previous liver pathologies.
Consumers and health professionals are encouraged to report adverse reactions with withania to the TGA.
https://www.tga.gov.au/safety/reporting-problems
Scandinavia bans withania
Danish authorities have long sought to ban withania. I was part of a group making submissions on behalf of companies and practitioners to lift the restrictions to no avail.
Denmark prohibited ashwagandha due to safety worries regarding dosage in April 2023. This action was influenced by a 2020 Danish Technical University study indicating potential adverse effects on thyroid and sex hormones, including a possible link to abortions. While the instances of hormone issues noted in the study were uncommon, there was no confirmed clinical proof of ashwagandha causing abortions. With safety as a priority, Denmark opted to ban ashwagandha entirely, prompting other Nordic nations to contemplate similar actions.
Idiosyncratic drug-induced liver injury (DILI)
Idiosyncratic drug-induced liver injury (DILI) is a rare but significant cause of liver problems. Recently, new triggers of DILI have been identified, such as COVID vaccines, turmeric, green tea extract, and immune checkpoint inhibitors. Diagnosing DILI typically involves ruling out other common causes of liver damage and establishing a clear link between the suspected drug and the onset of symptoms. Advances in assessing DILI causality now include the development of a semi-automated tool called the revised electronic causality assessment method (RECAM). Furthermore, specific genetic associations with certain drugs have been found to aid in confirming or ruling out DILI in individual patients. Prognostic models are available to help identify patients at the highest risk of death, around 5% to 10%. Most patients recover fully after stopping the offending drug, but 10% to 15% may still have abnormal liver tests after six months. Hospitalized patients with severe DILI may benefit from N-acetylcysteine therapy or urgent liver transplant evaluation if they show specific signs. Some patients with certain features on liver biopsy might benefit from short-term corticosteroids. However, more research is needed to determine the best approach regarding patient selection, dosage, and duration of steroid treatment(Fontana et al., 2023).
Population-based studies from France and Iceland estimate the annual incidence of DILI to be 14–19 cases per 100,000 inhabitants. Lower incidence rates have been reported in the United States and higher rates in China (Fontana et al., 2023).
Paediatric patients account for 5%–10% of patients with DILI and children seem to be at increased risk for valproate and minocycline hepatotoxicity, whereas the elderly are more susceptible to isoniazid and amoxicillin-clavulanate (AC) hepatotoxicity (Fontana et al., 2023). Women seem to experience more frequent and severe hepatotoxicity particularly from diclofenac, interferon-β1a, and nitrofurantoin, whereas men seem to be more susceptible to azathioprine, anabolic steroid, and AC DILI. AC is the most common cause of DILI in western patients with an estimated incidence of 1 in every 2500 users of AC (Fontana et al., 2023).
Herbal and dietary supplements including green tea, withania, Garcinia cambogia, and curcumin are the leading cause of DILI in Asian countries, such as China and Korea. They have also been increasingly reported in western countries, accounting for nearly 20% of cases in the Drug Induced Liver Injury Network (DILIN) (Fontana et al., 2023).
RUCAM
The modified Rousell Uclaf causality assessment method (RUCAM) and revised electronic causality assessment method (RECAM) are structured causality assessment instruments that provide a numerical score based on points assigned for diagnostic testing, temporal association, and other clinical features that can be used by both expert and practicing clinicians. The CIOMS/RUCAM scale has been proposed to establish causal relationship between offending drug and liver damage. The CIOMS/RUCAM scale involves a scoring system which categorizes the suspicion into "definite or highly probable" (score > 8), "probable" (score 6-8), "possible" (score 3-5), "unlikely" (score 1-2) and "excluded" (score ≤ 0). In clinical practice physicians put more emphasis on the presence or absence of similarity between the biochemical profile of the patient and known biochemical profile of the suspected toxicity ( e.g. cholestatic damage in amoxycillin-clauvonic acid ).
Cases of suspected withania-induced hepatotoxicity 2017 to 2023
Several cases of liver toxicity resulting from commercially available Ashwagandha products have been reported. The first report of Ashwagandha-related liver damage was from Japan, which was quickly resolved after drug-withdrawal. Later, similar cases of liver toxicity due to Ashwagandha consumption were reported from the USA and Iceland.
Withanone (one of the withanolides) is found in significant amounts in Ashwagandha extracts (19 and 3Â mg/g dry weight of leaves and roots, respectively) and is thought to be responsible for many of its medicinal properties.
There have been several cases of liver toxicity resulting from commercially available Ashwagandha products. The symptoms usually resolve with discontinued use and fatalities or chronic injuries have not been reported.
Japan – Inagaki et al 2017
The initial documentation of potential drug-induced liver damage linked to Ashwagandha originated in Japan. A 20-year-old man with social-anxiety disorder was admitted for liver dysfunction accompanied with hyperbilirubinemia. He had used ashwagandha which he imported online in combination with multiple anti-anxiety drugs on his own judgment. He had taken more than twice the recommended dosage for one month before hospitalization. Drug-induced liver injury classified as hepatocellular type by Ashwagandha was suspected, due to a score of 8 that is "high possibility" by the DDW-J 2004 DILI diagnostic criteria. Hyperbilirubinemia became exacerbated despite the cessation of ashwagandha and concomitant drugs. Histological findings revealed many canalicular bile plugs. His liver function was normalized after initiation of ursodeoxycholic acid and phenobarbital within two months. A drug-induced lymphocyte stimulation test revealed reactivity and drug interactions between Ashwagandha, propranolol, and alprazolam (Inagaki et al., 2017).
Iceland and US Drug-Induced Liver Injury Network 2020
Björnsson et al. 2020 reported on five cases of liver injury attributed to ashwagandha-containing supplements. Three were collected in Iceland during 2017-2018 and two were collected from the Drug-Induced Liver Injury Network (DILIN) in 2016. Other causes for liver injury were excluded. Causality was assessed using the DILIN structured expert opinion causality approach. Among the five patients, three were males; mean age was 43 years (range 21-62). All patients developed jaundice and symptoms such as nausea, lethargy, pruritus and abdominal discomfort after a latency of 2-12 weeks. Liver injury was cholestatic or mixed (R ratios 1.4-3.3). Pruritus and hyperbilirubinaemia were prolonged (5-20 weeks). No patient developed hepatic failure. Liver tests normalized within 1-5 months in four patients. One biopsy was performed, showing acute cholestatic hepatitis. Chemical analysis confirmed ashwagandha in available supplements; no other toxic compounds were identified. No patient was taking potentially hepatotoxic prescription medications, although four were consuming additional supplements, and in one case, rhodiola was a possible causative agent along with ashwagandha. Liver injury is typically cholestatic or mixed with severe jaundice and pruritus, but self-limited with liver tests normalizing in 1-5 months (Bjornsson et al., 2020).
UK Ireland et al. 2021
A 39-year-old female presented with a one-week history of jaundice and nausea after taking an over-the-counter herbal supplement containing ashwagandha root extract. Initial investigations revealed a hepatocellular pattern of liver enzyme abnormality with jaundice. Investigations, including viral serology, liver specific autoantibodies and an ultrasound scan of the abdomen, were unremarkable. Liver biopsy showed an acute cholestatic hepatitis with confluent necrosis but no features of chronicity. The patient received treatment with ursodeoxycholic acid (Ireland et al., 2021).
USA Waller et al
A 20-year-old male with Hodgkin’s lymphoma in remission, anxiety, and depression, presented to clinic with 2-weeks of generalized pruritus, dark urine, and pale, greasy bowel movements. He had associated chills, fatigue, nausea, and decreased appetite with an 8 lb weight loss. He denied abdominal pain, scleral icterus, vomiting, or swelling. Medications included Alprazolam 0.5mg PRN, Clonazepam 1mg QHS, Desvenlafaxine ER 150mg daily, Guanfacine 1.5mg daily, Lurasidone 160mg daily, Omeprazole 20mg daily, and Risperidone 0.25mg PRN.
Upon further questioning, the patient disclosed that upon recommendation from his psychiatric provider, his mother ordered the â€NOW†brand â€standardized extract†Ashwagandha supplement 450mg as an adjuvant therapy for his anxiety. He had been taking the supplement 1-2 times daily for 4 weeks prior to the onset of symptoms. Physical examination showed a young male in mild distress with visible excoriations, no jaundice or organomegaly. The remainder of the exam was unremarkable. Lab work revealed normal complete blood count, ESR and electrolytes. Total bilirubin was 1.5, AST 514, ALT 955 and bile acids were elevated. A screening panel for EBV, Hepatitis A, B and C was negative. Ashwagandha was discontinued. Within two weeks, the pruritus and additional symptoms had significantly improved, and the total bilirubin and liver enzymes were down trending. One month after discontinuation, the total bilirubin was 0.4, AST 36, ALT 64 (Waller et al., 2021).
Bokan et al. 2022
Bokan et al. 2022 reviewed the ten previously cases and reported on two new cases of potential ashwagandha hepatotoxicity. In the first case, a 36-year-old man used ashwagandha capsules (450 mg, three times daily) for 6 months before he developed nausea, pruritus, and dark-coloured urine. In the second case, a 30-year-old woman developed pruritus after 45 days of using ashwagandha capsules (450 mg). In both cases, serum bilirubin and liver enzymes (aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP) were increased. The liver injury pattern was hepatocellular (R-value 11.1) and mixed (R-value 2.6), respectively. The updated Roussel Uclaf Causality Assessment Method (RUCAM) indicated a "probable" relationship with ashwagandha with a score of seven. Clinical and liver function improvements were observed after the discontinuation of ashwagandha supplement use (Bokan et al., 2023).
Ali et al. 2022
A 20-year-old healthy college student presented to our ER with complaints of yellowish discoloration of skin and worsening abdominal pain for 3 days. The discoloration was initially noted in his eyes, associated with excessive itching of skin but no stool changes. He also had right upper quadrant abdominal pain, 6/10 in intensity, without any associated aggravating or relieving factors. He denied recent travel, alcohol or drug consumption and his last sexual encounter was 4 months ago. His physical examination was significant for a normal BMI, icteric sclera, soft and non-tender abdomen. Initial labs showed AST of 659 and ALT of 415 and direct bilirubinemia of 8.6. A thorough autoimmune, infective hepatitis panel and haemolytic anaemia work up was negative. USG and CT abdomen/pelvis showed no abnormalities. He had been taking Ashwagandha 450mg every day for the past 30 days to “calm his nervesâ€. Over the course of his hospitalization, he symptomatically improved with down trending liver enzymes and bilirubin. He was advised to avoid ashwagandha containing supplements in the future. Post-discharge 3 week follow up showed a normal hepatic function test. The liver injury presents 2 to 12 weeks after ingestion with a cholestatic or mixed pattern of injury, jaundice and pruritus. Jaundice tends to be a dominant feature but ultimately resolves after discontinuation of the offending drug without fatalities or chronic injury (Ali et al., 2022).
USA Mohammad et al., 2022
A case of a 44-year-old Caucasian female with a past medical history of irritable bowel syndrome, anxiety, ADHD, herniated disc status post motor vehicle collision presenting to the emergency department for complaint of a one-month history of painless jaundice and pruritus. The patient was taking Xanax for anxiety and has been taking an herbal supplement for her stress relief. She notes that she was also evaluated in Florida and hospitalized with a negative ultrasound, MRCP, and hepatitis screening. She noted worsening jaundice, prompting her evaluation in the emergency department again. She also reported nonspecific abdominal discomfort. She stated that the herbal supplement she was taking composed of Ashwagandha and stopped taking the supplement since she noted her symptoms. The patient was prescribed cholestyramine for her itching. She discontinued taking any herbal supplement, such as Ashwagandha as this may have precipitated her underlying jaundice and liver disease (Mohammad et al., 2022).
Vaziarani et al. 2023
A 48-year-old man with a history of severe alcohol use disorder presented to the emergency department with jaundice, abdominal pain, dark urine, and pale stools after taking an over-the-counter testosterone-boosting supplement called TestBoost. The patient had withdrawal symptoms from alcohol and started the supplement to increase energy. His symptoms worsened after taking the supplement, leading to liver injury. Despite negative viral and autoimmune tests, the cholestatic injury was attributed to ashwagandha in the supplement. The patient's liver function improved after discontinuing the supplement but relapsed into alcohol use later. The patient's liver injury was likely due to a combination of factors, including repeated exposure to toxins from alcohol abuse. Diagnostic tools like RUCAM can help assess drug-induced liver injury (DILI) probability. The lack of standardized testing for supplements poses challenges in identifying harmful substances promptly (Vaziarani et al., 2023).
Spain Casiano-Manzano et al. 2023
A 33-year-old male with an unremarkable medical history was admitted to the Gastroenterology Department. He presented with pruritus, jaundice, and choluria that had appeared over several days. Blood tests revealed elevated total bilirubin levels (10.7mg/dl), direct bilirubin (6.27 mg/dl), and increased transaminases. The alanine aminotransferase/alkaline phosphatase (ALT/ALP) ratio (R) suggested cholestatic liver damage. The patient reported no medication, alcohol, or drug use but acknowledged consuming ashwagandha to manage stress. Comprehensive tests ruled out other liver diseases. The patient improved, and bilirubin levels decreased to 4.5mg/dl before discharge. A month later, the patient returned with deteriorating jaundice, choluria, pruritus, and weight loss. Blood tests showed elevated bilirubin (total bilirubin 21.1mg/dl and direct bilirubin 15.3mg/dl) and ALP, with a mild increase in transaminases. The patient had ceased ashwagandha use for two months and denied using any other hepatotoxic substances. The RUCAM scale scored 8 and classified the case as a probable herb induced liver injury (HILI) due to ashwagandha. While the patient initially deteriorated, corticosteroid treatment led to significant improvement (Casiano-Manzano et al., 2023).
India Suryawanshi et al., 2023
Ashwagandha-Associated Acute Liver Failure Requiring Liver Transplantation(Suryawanshi et al., 2023)
Dhaliwal et. Al 2023
The patient was a 22-year-old male who presented with worsening jaundice, pruritus, and fatigue for 1 month. He reported a 2-week usage of Ashwagandha. He began to experience mild symptoms that peaked at around 6 weeks after initial use. On arrival, he had mild tachycardia and tachypnea with a benign exam. Labs were notable for total bilirubin (TB) 28.3, direct bilirubin (DB) 25, ALP 362, AST 52, and ALT 64 with normal coagulation parameters. Lab results were TB 31.0, DB 21.19, ALP 434, AST 439, and ALT 437. A hepatitis panel, HIV, and mononucleosis screen were all negative. Ultrasound and MRCP were unremarkable. Further questioning revealed that the patient was taking Ashwagandha daily for 2 weeks before symptom onset. The patient was started on symptomatic management with hydroxyzine. Over the next 2 days, the patient reported symptomatic improvement with improving liver enzymes. He was discharged with recommendations for repeat labs outpatient and strict avoidance of Ashwagandha (Dhaliwal et al., 2023).
Poland Lubarska et al., 2023
A 23-year-old male presented with jaundice and elevated liver enzymes after consuming ashwagandha supplements, leading to acute hepatitis. Diagnostic tests ruled out viral causes and autoimmune conditions, with subsequent treatment and discontinuation of ashwagandha resulting in normalized liver function. The patient reported pruritus, malaise, fatigue, gastrointestinal disorders, and stool discoloration. The patient did not take any medications regularly. He had been recently consuming ashwagandha dietary supplements (the dose and quality of the supplement are unknown). Serological tests for viral hepatitis were ordered and viral aetiology was excluded. During hospitalization, a further increase in the concentration of bilirubin, and thus a significant intensification of pruritus, was observed. Treatment with methylprednisone, ornithine aspartate, ursodeoxycholic acid, potassium, hyoscine, and lactulose was introduced. Due to abnormal liver tests and particularly high total bilirubin concentrations, a Sheldon catheter was placed, and plasmapheresis was performed four times. The Roussel Uclaf Causality Assessment Method (RUCAM) scale was used as the diagnostic algorithm for assessing the causality of liver damage. The RUCAM score obtained was six, consistent with probable ashwagandha-induced liver injury. Penicillamine and ursodeoxycholic treatments were implemented. After 3.5 months of intensive pharmacological treatment, plasmapheresis, and discontinuation of ashwagandha, liver tests and total bilirubin levels normalized. The patient’s general condition improved considerably. Major causes of liver damage were excluded, confirming that herbal supplements containing ashwagandha were most likely the causative agent of drug-induced liver injury (DILI) (Lubarska et al., 2023).
Germany Tóth et al., 2023
A 65-year-old woman was referred to the Department of Gastroenterology, Salem Medical Centre, Heidelberg, due to suspected toxic hepatitis. On admission, the patient had jaundice of the skin and sclera without any abdominal pain. She reported a weight loss (3 kg in 3 weeks) as well as diarrhea (about 4 times/day) with pale stool and dark urine during the last 3 weeks The patient developed jaundice 2 weeks after starting ashwagandha intake and recovered within 5 months after withdrawal without any specific treatment (Tóth et al., 2023).
Lareb case reports 2023
Lareb reported on four reports of liver toxicity associated with the use of products that contain Ashwagandha. In two reports only Ashwagandha was used and in the other two reports multiple herbs were used. In one of these reports Scutellaria baicalensis was also used, which also been implicated in causing liver injury. Time to onset varied from three months to ten months. The latency of drug induced liver injury is typically between five days and three months of starting a medication. Measurement of time to onset, however, may be difficult. The latency is usually measured from the time of starting to the time of onset of jaundice, dark urine or detection of an elevation in serum bilirubin; but in other situations, latency is measured to the time of the first symptom, which might be fatigue, weakness, nausea, poor appetite, abdominal pain, fever, rash or itching. Three patients reported to have withdrawn the Ashwagandha containing product and of one patient the action taken is unknown, and all patients were recovering at the time of reporting. Typically, improvement of drug induced liver injury starts within a week or two of stopping therapy, and the injury resolves completely within 2 to 3 months. For the determination of the RUCAM score, age ≥ 55 years is a risk factor for liver injury. Three of the four patients in the reports received by Lareb were younger. Several cases of clinically apparent liver injury have been reported in the literature of patients taking commercial herbal products that are labelled as containing Ashwagandha. It is important to note that commercial herbal preparations are often mixtures of herbs and nutritional products and can be mislabelled and contain unknown herbs and medications. Therefore, it cannot be totally ruled out that reported cases are due to a contaminant (Lareb, 2023).
References
Ali, S. M. J., Suresh, M. G., Sanchez-Cruz, J., & Anand, C. (2022). S2976 Cry Me a Liver: Ashwagandha-Induced Liver Toxicity. Official journal of the American College of Gastroenterology | ACG, 117(10S), e1931. https://doi.org/10.14309/01.ajg.0000868544.04043.fe
Bjornsson, H. K., Bjornsson, E. S., Avula, B., Khan, I. A., Jonasson, J. G., Ghabril, M., Hayashi, P. H., & Navarro, V. (2020). Ashwagandha-induced liver injury: A case series from Iceland and the US Drug-Induced Liver Injury Network. Liver Int, 40(4), 825-829. https://doi.org/10.1111/liv.14393
Bokan, G., Glamocanin, T., Mavija, Z., Vidovic, B., Stojanovic, A., Bjornsson, E. S., & Vucic, V. (2023). Herb-Induced Liver Injury by Ayurvedic Ashwagandha as Assessed for Causality by the Updated RUCAM: An Emerging Cause. Pharmaceuticals (Basel), 16(8). https://doi.org/10.3390/ph16081129
Casiano-Manzano, S., Torres-Larrubia, M., Masa-Caballero, A., Jimenez-Colmenarez, Z., Martin-Noguerol, E., Fernandez-Bermejo, M., & Solis-Munoz, P. (2023). Changing perspectives: unveiling the risks of ashwagandha-induced hepatotoxicity. Rev Esp Enferm Dig. https://doi.org/10.17235/reed.2023.10080/2023
Dhaliwal, G., Hussain, M., & Sivanandham, R. (2023). P3937 - From Herb to Harm: A Rare Encounter of Ashwagandha-Induced Liver Injury, ACG 2023 Annual Scientific Meeting Abstracts. Vancouver, BC, Canada: American College of Gastroenterology.
Fontana, R. J., Bjornsson, E. S., Reddy, R., & Andrade, R. J. (2023). The Evolving Profile of Idiosyncratic Drug-Induced Liver Injury. Clinical Gastroenterology and Hepatology, 21(8), 2088-2099. https://doi.org/https://doi.org/10.1016/j.cgh.2022.12.040
Inagaki, K., Mori, N., Honda, Y., Takaki, S., Tsuji, K., & Chayama, K. (2017). A case of drug-induced liver injury with prolonged severe intrahepatic cholestasis induced by Ashwagandha. Kanzo, 58(8), 448-454. https://doi.org/10.2957/kanzo.58.448
Ireland, P. J., Hardy, T., Burt, A. D., & Donnelly, M. C. (2021). Drug-induced hepatocellular injury due to herbal supplement ashwagandha. J R Coll Physicians Edinb, 51(4), 363-365. https://doi.org/10.4997/JRCPE.2021.409
Lareb. (2023). Netherlands Pharmacovigilance Centrem https://www.lareb.nl/en/news/liver-toxicity-associated-with-products-containing-ashwagandha-1?query=#:~:text=Pharmacovigilance%20centre%20Lareb%20received%20four,toxicity%20when%20using%20these%20products.
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Mohammad, R., Eric, M., E., J., Lucerna, A., & Neeharika, B. (2022). "An Herbal Liver Effect: Ashwagandha-Induced Hepatotoxicity" (2022). Stratford Campus Research Day. 14. https://rdw.rowan.edu/stratford_research_day/2022/May5/14
Suryawanshi, G., Abdallah, M., Thomson, M., Desai, N., Chauhan, A., & Lim, N. (2023). Ashwagandha-Associated Acute Liver Failure Requiring Liver Transplantation. American Journal of Therapeutics, 30(1), e80-e83. https://doi.org/10.1097/mjt.0000000000001466
Tóth, M., Benedek, A. E., Longerich, T., & Seitz, H.-K. (2023). Ashwagandha-induced acute liver injury: A case report. Clinical Case Reports, 11(3), e7078. https://doi.org/https://doi.org/10.1002/ccr3.7078
Vaziarani, S., Kothari, A., Fujimoto, J., & Gomez, M. (2023). Supplements Are Not a Synonym for Safe: Suspected Liver Injury From Ashwagandha. Fed Pract., 9.
Waller, S., Wong, T. H., & Dannenhoffer, R. (2021). Youngest reported case of liver injury related to Ashwagandha. Authorea.