Millions of Americans swallow turmeric capsules, green tea extract pills, and ashwagandha tablets each day with no warning label about liver damage. Between 2004 and 2013, the share of drug-induced liver injury cases tied to herbal and dietary supplements nearly tripled in the only prospective U.S. registry tracking such harm. The rise happened quietly, with most patients unaware their supplement was the cause until symptoms mimicked hepatitis or worse.
Why the surge in botanical liver injuries demands attention now
The Drug-Induced Liver Injury Network, a federally funded prospective registry, enrolled cases from 2004 to 2013 and found that the proportion of cases attributed to herbal and dietary supplements rose from 7% to 20% during that period. That shift outpaced many conventional prescription drugs in the same registry. The trend has not been tracked with the same rigor since, because no updated prospective registry data covering the years after 2013 have been published in primary sources. Supplement sales, meanwhile, have continued to climb, expanding the population potentially exposed to poorly characterized risks.
The gap between exposure and documented harm is at the center of an ongoing debate. The American Botanical Council issued a statement calling a JAMA-linked exposure study an exaggeration of liver injury risk, arguing that broad population exposure estimates should not be conflated with confirmed cases of organ damage. That distinction matters: if tens of millions of people take a supplement and only dozens suffer acute injury, the absolute risk per user is small. But for the individuals who develop liver failure weeks after starting a new bottle, the consequences are severe and often misdiagnosed, especially when products are marketed as “natural” and therefore assumed to be benign.
One hypothesis gaining traction among hepatologists centers on a specific genetic marker. Research on green tea extract cases within a prospective U.S. framework identified a strong association between the HLA-B*35:01 allele and liver injury. Carriers of this allele appear far more susceptible to hepatotoxicity from certain botanical products. If a similar genetic vulnerability applies to turmeric and curcumin formulations, especially those engineered for higher bioavailability, it could explain why a small subset of users suffers disproportionate harm while most experience none. Testing that idea would require matching product-specific exposure data with genetic profiles in new registry cases, a step that has not yet been completed and would demand coordinated funding, genotyping, and systematic product collection.
Registry data, LiverTox records, and product variability
The strongest clinical evidence comes from two types of records. The DILIN registry data, published in Hepatology, captured real-world severity across hundreds of enrolled cases and showed herbal supplements steadily gaining ground as a cause of liver injury relative to conventional medications. Separately, the National Institutes of Health LiverTox database, a curated clinical reference, documents that turmeric and curcumin supplements have been implicated in several dozen cases of clinically apparent acute liver injury. Many of those cases involved newer formulations designed to boost absorption of curcumin, which is poorly absorbed on its own, raising the possibility that enhanced bioavailability may increase the risk of idiosyncratic reactions.
Green tea extract tells a parallel story. LiverTox case syntheses describe an acute hepatitis-like syndrome appearing weeks after patients begin concentrated extract capsules, distinct from brewed tea consumption. A United States Pharmacopeia review examined published case reports and identified significant variability in product chemistry and manufacturing controls across brands, suggesting that not all green tea supplements carry equal risk. Some products contain highly standardized catechin concentrations, while others combine green tea with multiple stimulants or weight-loss agents, complicating attribution when liver tests suddenly spike.
Ashwagandha has drawn attention more recently, with case clusters showing a cholestatic or mixed pattern of liver injury, typically appearing weeks after first use and sometimes accompanied by intense itching and jaundice. Garcinia cambogia, a common weight-loss ingredient, triggered regulatory concern during the Hydroxycut recalls and continues to appear in case reports involving multi-ingredient formulas, where it is difficult to separate the effects of each component. In many of these products, labels list a proprietary blend without specifying exact amounts, making dose–response relationships nearly impossible to establish.
Black cohosh presents a different challenge. Numerous liver injury reports exist, but some implicated products were later found to contain other Actaea species rather than Actaea racemosa, the intended botanical. That misidentification problem makes it difficult to assign blame to the plant itself versus contaminated or adulterated products, a distinction that applies broadly across the supplement market. When a capsule contains the wrong species, undeclared pharmaceuticals, or concentrated extracts far stronger than traditional preparations, the term “herbal” obscures more than it explains.
Gaps in tracking, genetics, and what consumers should watch
Several critical questions remain open. No primary national survey or exposure dataset has been published that precisely quantifies how many Americans currently take the specific botanicals most often linked to liver injury. The figure of nearly 16 million referenced in recent coverage draws on broad supplement-use surveys, but matching those users to the exact products and formulations implicated in liver cases has not been done at scale. Without that linkage, risk estimates remain crude, and debates over whether the hazard is being overstated or understated are difficult to resolve empirically.
The DILIN registry, the best prospective tool available, has not published updated proportional data beyond its 2004 to 2013 enrollment window. Whether the herbal share of liver injury cases has continued rising, plateaued, or shifted to different products is unknown from primary sources. Chemical analysis of specific implicated products is also absent from most LiverTox case syntheses, leaving open questions about whether contaminants, undisclosed drugs, or manufacturing changes are driving some of the most severe events. For now, clinicians must rely on careful histories, pattern recognition, and exclusion of other causes rather than definitive toxicology.
Genetic research adds another layer of uncertainty. The association between HLA-B*35:01 and green tea–related injury suggests that a small fraction of the population may be at outsized risk from certain botanicals, but routine screening is not available, and the allele’s role in other supplement injuries has not been fully explored. If future studies confirm similar markers for turmeric, ashwagandha, or other popular products, regulators and manufacturers will face difficult questions about whether to recommend targeted testing, add specific warnings, or reformulate high-exposure products.
For consumers, the practical steps are more straightforward than the science. People with existing liver disease, those taking multiple prescription medications, and individuals who drink heavily or have a history of unexplained jaundice should approach concentrated botanical supplements with particular caution. Any new onset of fatigue, dark urine, abdominal pain, or yellowing of the eyes in the weeks after starting a supplement warrants prompt medical evaluation and disclosure of all nonprescription products, including those marketed as natural or traditional.
Clinicians, meanwhile, are being urged by hepatology experts to ask explicitly about herbal and dietary supplements when evaluating abnormal liver tests, rather than assuming prescription drugs or viral infections are the only plausible culprits. Rapid recognition and withdrawal of a suspect product can mean the difference between full recovery and progression to liver failure. Reporting suspected cases to registries and pharmacovigilance systems, when available, helps fill the data gaps that currently obscure the true scope of the problem.
The science around botanical liver injury remains incomplete, but the signal is strong enough to justify vigilance. Concentrated extracts of plants long used in food or traditional medicine are not inherently safe simply because they are derived from nature. Until exposure data, genetic insights, and rigorous product testing catch up with consumer demand, both patients and clinicians will be navigating a landscape where serious but uncommon risks coexist with widespread, largely unmonitored use.
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*This article was researched with the help of AI, with human editors creating the final content.
