Ashwagandha and Liver Injury: The Case Reports Behind the TGA Safety Signal
Australia's TGA updated its ashwagandha safety advisory in July 2026. Here's what the underlying case reports, LiverTox data, and causality assessments actually show.
Medical disclaimer: This article is written for educational and informational purposes only. It does not constitute medical advice, diagnosis, or treatment. Anyone experiencing jaundice, dark urine, pale stools, unexplained fatigue, or abdominal pain while taking any supplement should stop use and seek medical attention. This article does not recommend for or against ashwagandha use; it summarises the published safety evidence.
What Happened
On 7 July 2026, Australia's Therapeutic Goods Administration issued an updated safety advisory on Withania somnifera (ashwagandha), reporting that it had now received 11 case reports of possible ashwagandha-related liver injury since it opened its original safety review in 2021 and first advised on the risk in 2024. Four of those reports were new since the 2024 advisory. Of the 11, the TGA assessed six as having no other ingredient plausibly responsible for the liver injury, and four of those six involved products listed on Australia's therapeutic goods register, with two requiring hospitalisation. No deaths or liver transplants have been reported among the Australian cases. The regulator's own framing, as reported by the industry trade press that covered the update, was that "the available evidence indicates that while the risk appears to be very rare, there is a potential for liver injury associated with this herbal ingredient," and that it would continue assessing the evidence to decide whether further regulatory action is warranted (Nutra Ingredients, 20 July 2026). India's regulator moved further in April 2026, restricting ashwagandha use to root and root-extract material and prohibiting leaf and leaf-extract use in supplements, a distinction that turns out to matter mechanistically (see below).
This is a genuinely new development in the ashwagandha evidence base, not a repeat of the concerns already covered in our cognitive and anxiolytic evidence review of the compound. This article goes deeper into the specific case report literature and the causality science behind the TGA's signal, since anyone using ashwagandha as a cognitive or stress-management nootropic should understand what the injury pattern actually looks like, how rare it really is, and which product characteristics the evidence points to as higher risk.
The Published Case Literature
Ashwagandha-associated liver injury was first reported in the medical literature in 2017 and case reports have accumulated steadily since. A 2023 causality review using the updated Roussel Uclaf Causality Assessment Method (RUCAM), the standard clinical tool for attributing liver injury to a specific drug or herbal exposure, identified 10 previously published cases across six articles and added two new ones of its own, for a total of 12 documented cases assessed with a structured methodology. Both of the newly reported cases scored 7 on the RUCAM scale, corresponding to a "probable" causal relationship once other causes (viral hepatitis, autoimmune disease, other medications, biliary obstruction) had been excluded through serology and imaging (Bokan G et al., Pharmaceuticals 2023;16(8):1129).
A representative case from this literature: a 65-year-old woman began taking ashwagandha for "troubled thoughts" and developed jaundice two weeks later, with markedly elevated bilirubin, weight loss, pale stools, and dark urine. Liver biopsy showed hepatocellular and canalicular cholestasis with spotty necrosis, a pattern consistent with drug-induced injury rather than viral or autoimmune hepatitis. She recovered over five months after stopping the supplement, with no specific treatment beyond supportive care for pruritus (Tóth M et al., Clin Case Rep 2023;11(3):e7078).
LiverTox, the NIH's clinical reference database on drug-induced liver injury, classifies ashwagandha at a Category B likelihood score: a "likely cause of clinically apparent liver injury" when other causes have been excluded, based on roughly two dozen published cases as of its most recent update. The typical latency is 2 to 12 weeks after starting the supplement, though cases have been reported as early as 3 days and as late as 12 months in. The dominant injury pattern is cholestatic or mixed hepatocellular-cholestatic, presenting as jaundice and pruritus that is usually self-limiting but can be protracted. Rare fatal cases and cases requiring liver transplantation have occurred, overwhelmingly in patients who already had cirrhosis or advanced liver disease before starting ashwagandha, a population LiverTox explicitly advises should avoid the supplement entirely. Rechallenge, restarting ashwagandha after a documented injury episode, is considered contraindicated once a case has occurred (LiverTox: Ashwagandha, NIH National Library of Medicine, last updated December 2024).
Why This Happens: The Leading Mechanistic Hypothesis
The exact mechanism of ashwagandha-induced liver injury is not settled, but the leading suspects are the withanolides, the same steroidal lactone class responsible for the compound's anxiolytic and cognitive effects. LiverTox specifically flags withanone, a related metabolite, for its capacity to form DNA adducts that could interfere with normal transcription and replication in hepatocytes, a plausible if unconfirmed route to idiosyncratic hepatotoxicity. Idiosyncratic in this context means the injury does not track a simple dose-response curve the way paracetamol overdose does. It appears to depend on some combination of individual susceptibility and product-specific factors, which is consistent with the injury remaining rare relative to the very large number of people taking ashwagandha supplements without incident.
Product quality is a recurring theme in the case literature. Several reviews note that mislabelling, contamination, and undeclared adulteration in commercial ashwagandha products are a persistent confound, since a liver injury attributed to "ashwagandha" in a case report may in some instances reflect an unlisted co-ingredient rather than the withanolide fraction itself. This is one reason the RUCAM-scored cases (which formally excluded alternative causes) carry more evidential weight than raw adverse event counts.
The root-versus-leaf distinction that has driven the regulatory divergence between Australia and India is grounded in withanolide chemistry. Leaf material contains substantially more withaferin A relative to root-derived extracts, and withaferin A is the withanolide most associated with hepatocyte toxicity in cell culture models at concentrations achievable through supplementation. Root-only extracts, including the widely studied KSM-66 formulation discussed in our companion review, are lower in withaferin A and higher in withanolide A, which has not shown the same hepatotoxic signal in vitro. This is the same distinction our existing ashwagandha review already flags as a reason to prefer root-only extracts, and the TGA's 2026 safety advisory alongside India's parallel regulatory action, detailed in the Nutra Ingredients coverage of both actions, gives that recommendation considerably more regulatory weight than it had when the clinical trial literature alone was the only consideration.
How Rare Is "Very Rare"
Putting the numbers in context matters here, because a handful of case reports against a very large user base can be read in two opposite and equally misleading ways: as proof the risk is negligible, or as proof of a hidden epidemic. Neither is accurate.
Ashwagandha is one of the most widely used adaptogenic supplements globally, with usage almost certainly in the millions of person-years when trial participants and commercial consumers are combined. Eleven reports of possible injury reaching the TGA over roughly five years of active safety monitoring, against that user base, is consistent with the regulator's own description of the risk as "very rare." The LiverTox count of approximately two dozen published cases globally, accumulated over nearly a decade of case report literature, tells the same story: this is a real signal, established through structured causality assessment in at least a dozen cases, but it is not a common event, and the large randomised controlled trials of ashwagandha for cognition and stress, including the Chandrasekhar 2012 and Choudhary 2017 trials discussed in our companion evidence review, reported no clinically significant hepatic adverse events among several hundred combined participants over 8 to 12 week durations.
What has changed since 2024 is not the size of the risk so much as the confidence in its reality. A single case report is weak evidence for causality. A dozen independently reported cases, several formally adjudicated with RUCAM scoring against excluded alternative causes, and a regulator tracking a rising count over a defined monitoring period, is a materially stronger evidentiary position, even though the absolute numbers remain small.
Practical Implications for Nootropic Use
None of this evidence supports blanket avoidance of ashwagandha for the general population, and the TGA's own framing does not call for that either. It does support several concrete, evidence-grounded adjustments for anyone using ashwagandha as part of a cognitive or stress-management protocol:
Preexisting liver disease is the clearest contraindication. The rare severe outcomes in the case literature, including the transplant cases, cluster overwhelmingly in people with pre-existing cirrhosis or chronic liver disease. This population should avoid ashwagandha entirely, a recommendation both LiverTox and our existing evidence review already make and that the 2026 case accumulation reinforces rather than changes.
Root-only, standardised extracts carry the more favourable chemistry. Given the withaferin A signal in leaf material, choosing extracts specified as root-only (KSM-66 is the most extensively trial-tested example) over leaf-containing or unspecified "full-spectrum" products is a reasonable precaution, independent of any effect on efficacy.
Watch for the specific symptom pattern, not vague malaise. Jaundice, dark urine, pale stools, pruritus, and unexplained fatigue appearing within the first weeks to months of starting ashwagandha is the pattern documented across the case series. These are specific, recognisable symptoms rather than the kind of nonspecific fatigue that makes many supplement side effects hard to attribute. Anyone experiencing this pattern should stop the supplement and seek liver function testing rather than waiting to see if symptoms resolve.
Rechallenge is not advisable. If a liver injury episode has occurred and been attributed to ashwagandha, the case literature and LiverTox both treat restarting the supplement as contraindicated given the idiosyncratic injury pattern.
For readers weighing alternatives, our rhodiola rosea evidence review covers a mechanistically distinct adaptogen with a long clinical safety record and no comparable hepatotoxicity signal in the published literature, though it carries its own distinct interaction profile with serotonergic medications.
Summary
The TGA's July 2026 update does not overturn the clinical trial evidence for ashwagandha's cognitive and anxiolytic effects, and it does not establish that ashwagandha is broadly unsafe. What it does is confirm, with a growing and increasingly well-characterised case series, that a rare but real hepatotoxic signal exists, that it follows a recognisable cholestatic injury pattern with a 2-to-12-week latency, that it is mechanistically linked to the withanolide fraction and specifically implicates leaf material more than root, and that people with existing liver disease face a materially higher risk than the general supplement-using population. The appropriate response to this evidence is the same one that governs how this site treats every compound: match the confidence of the claim to the strength of the underlying data, favour root-only standardised extracts with the stronger trial base, and treat unexplained jaundice or dark urine during supplementation as a reason to stop and seek medical evaluation, not a reason to wait it out.
Primary and clinical references: Therapeutic Goods Administration, "Withania somnifera (Ashwagandha) and very rare risk of liver injury," safety update, 7 July 2026, as reported in Nutra Ingredients, 20 July 2026; Bokan G, Glamočanin T, Mavija Z, Vidović B, Stojanović A, Björnsson ES, Vučić V. "Herb-Induced Liver Injury by Ayurvedic Ashwagandha as Assessed for Causality by the Updated RUCAM: An Emerging Cause." Pharmaceuticals (Basel) 2023;16(8):1129; Tóth M, Benedek AE, Longerich T, Seitz H-K. "Ashwagandha-induced acute liver injury: A case report." Clin Case Rep 2023;11(3):e7078; LiverTox: Clinical and Research Information on Drug-Induced Liver Injury, "Ashwagandha," National Institute of Diabetes and Digestive and Kidney Diseases, National Library of Medicine, last updated December 2024. This article summarises published case reports and regulatory communications; it is not a substitute for individualised medical advice.