Ashwagandha and the liver: two case series, and what a reader should watch for

By the Jelly Force TeamLast updated September 20268 min readSafety · Reviewed by Dr. Dean Tomlin

This is a safety article about an ingredient on the bottle this website sells, and it exists because the finding is documented in two countries, is easy to act on, and is almost never mentioned on a page like this one.

Why an uncommon problem gets an article

Ashwagandha is one of the most widely used botanicals on this label and probably the most widely used adaptogen on any shelf. Its efficacy literature is reasonable: nine randomised trials pooled in 2024 found consistent effects on perceived stress, on the Hamilton Anxiety Scale and on serum cortisol (Arumugam 2024).

Widely used means widely exposed, and a rare event in a large population is still a real number of people. The signal described below is uncommon. It is also specific enough that a reader who knows what to look for can act on it within a day, which is the entire reason to write it down.

Five patients, Iceland and the United States

The first series was published in Liver International in 2020 and collected five cases attributed to ashwagandha-containing supplements: three from Iceland in 2017 and 2018, and two from the United States Drug-Induced Liver Injury Network in 2016 (Bjornsson 2020). Other causes of liver injury were excluded, and causality was assessed using a structured expert opinion approach.

The clinical picture, in the paper's own terms. Mean age 43, range 21 to 62; three of the five were men. All five developed jaundice. Symptoms included nausea, lethargy, itching and abdominal discomfort. Latency between starting the supplement and becoming ill ran two to twelve weeks.

The injury pattern was cholestatic or mixed rather than the hepatocellular pattern most people picture, with R ratios between 1.4 and 3.3. Itching and raised bilirubin were prolonged, lasting five to twenty weeks. No patient developed hepatic failure. Liver tests normalised within one to five months in the four patients who were followed up.

Chemical analysis confirmed ashwagandha in the supplements that were available for testing, and no other toxic compound was identified. None of the patients was taking a potentially hepatotoxic prescription medicine, though four were taking additional supplements and in one case a second herb was a possible contributor.

Read off the abstract of the 2020 Liver International paper, linked in the sources below.

A second series, from a different country

A second case series with a literature review was published in Hepatology Communications in 2023, from India (Philips 2023). Two independent series, from populations that do not overlap, reporting the same pattern, is the point at which a signal stops being anecdote.

The United States National Center for Complementary and Integrative Health summarises the position in fewer words than either paper: ashwagandha has been linked to liver injury in a small number of reports.

What to watch for, and when to stop

The practical version fits in one paragraph, and it is the reason this article exists.

Stop and seek medical advice if, after starting any ashwagandha-containing product, you develop jaundice, dark urine, pale stools, persistent itching or pain under the right ribs. Ask for liver function tests, and say what you have been taking and for how long. Keep the bottle.

The latency window in the published series was two to twelve weeks, which means the relevant period is not the first few days. A symptom appearing in week six is squarely inside the described pattern.

• Jaundice: yellowing of the whites of the eyes or the skin
• Dark urine, or unusually pale stools
• Persistent itching with no rash to explain it
• Pain or discomfort under the right ribs
• Unexplained nausea and lethargy lasting more than a few days

How a case like this is actually attributed

It is worth understanding what a case series does and does not establish, because the phrase linked to gets used very loosely in this category in both directions.

Drug-induced liver injury is a diagnosis of exclusion. Other causes are ruled out first: viral hepatitis, alcohol, autoimmune disease, obstruction, and any prescription medicine with a known signal. The 2020 series states that this was done, and notes that none of the five patients was taking a potentially hepatotoxic prescription drug.

What is left is assessed for causality. The network the two American cases came from uses a structured expert opinion process, in which reviewers score the temporal relationship, the pattern of injury, the exclusion of alternatives and what happens when the agent is withdrawn. That last element is the strongest one available outside a deliberate re-challenge, which nobody performs for an ethical reason that is obvious.

Two complications are stated in the paper rather than hidden. Four of the five patients were taking additional supplements, and in one case a second herb was considered a possible contributor alongside ashwagandha. Chemical analysis confirmed ashwagandha in the products that were available, and no other toxic compound was identified in them.

So the honest reading is not that ashwagandha was proved to have caused five cases of liver injury. It is that five cases of a characteristic pattern were assessed by people whose job that is, alternatives were excluded, and ashwagandha was the most probable agent. A second independent series from India reporting the same pattern strengthens that considerably, because coincidence does not usually replicate across populations.

Keeping it in proportion

Two case series describing a handful of patients, set against an ingredient taken by very large numbers of people, is a small absolute risk. Nobody in the first series developed liver failure and everybody followed up recovered.

It is also worth noting where this bottle sits relative to the reports. The supplements in the published cases were ashwagandha products, and the ashwagandha fraction of an 82-milligram blend shared between nine names is small by any reading.

That is a reason to keep the risk in proportion, not a reason to leave it out. The honest position is that the signal is real, the amount here is small, and the signs are cheap to know.

The other interactions on this label

Green tea extract is the other name on this panel with a liver literature, and it belongs in an article like this one. A United States Pharmacopeia review ties the rare cases to intakes of 140 mg to about 1,000 mg of EGCG a day, and found that extract taken on an empty stomach raises EGCG exposure (Oketch-Rabah 2020); the whole blend in a gummy here is 82 mg. Horny goat weed, by contrast, has not been linked to liver injury, on the NIDDK’s own monograph (LiverTox).

Beyond the liver, four more interactions, each specific rather than general.

L-arginine widens blood vessels through the nitric oxide pathway, which means it adds to a nitrate or to a blood-pressure medicine. That is the single most important interaction on this bottle. In the pooled arginine trials (Rhim 2019) adverse effects ran at 8.3 per cent against 2.3 per cent on placebo, none of them severe.

Ashwagandha can add to a sedative, and it has thyroid activity in some people, which matters to anybody whose thyroid is already managed with a prescription.

Horny goat weed’s icariin inhibits PDE-5, the enzyme prescription tablets for erectile dysfunction block, in laboratory tests (Dell'Agli 2008), which makes that combination the one to settle before starting. And green tea has lowered blood levels of the blood-pressure drug lisinopril in volunteers (Misaka 2021).

Two of the nine names on this label, muira puama and catuaba, have thin enough human data that the honest answer about their interactions is that nobody knows. The side effects page covers all of this, including the tropane alkaloid question that sits behind the catuaba row.

One habit is worth more than all of this material put together, and it costs nothing. Keep a list of what you take, with the dates you started each thing, on your phone. If a symptom ever appears, that list is the first question anybody will ask you and the one most people cannot answer. Four of the five patients in the Icelandic and American series were taking more than one supplement, and the reason one of those cases carries a second possible agent is precisely that reconstruction after the fact is difficult.

The second habit is to introduce one thing at a time. A fortnight between new products is enough to attribute a reaction, and it costs a fortnight.

None of that is specific to this ingredient or to this bottle. It is what makes any supplement reaction traceable, and it is the difference between a case that teaches somebody something and a case that stays a shrug. The two series described above exist because five people and their clinicians could say what had been taken and when.