Milk thistle (silymarin) · The Ingredient Files

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Evidence by effect

Evidence strength (A–D, color) and effect size (dots, fill) are shown separately. The two axes are independent.

Claimed effect

Evidence strength

Effect size

One-line summary · key source

Reducing death or complications in alcoholic and viral (hepatitis B/C) liver diseaseEvidence type: Meta-analysis

D Insufficient

None

This directly rebuts the core of the 'good for the liver' belief. In a CochraneAn international network that rigorously reviews and synthesizes evidence. review pooling 18 randomized trials of milk thistle in 1,088 patients with alcoholic or hepatitis B/C liver disease, milk thistle had no significant effect versus placeboAn inert dummy treatment used as the comparison baseline. (or no intervention) on mortality (relative risk 0.78), complications of liver disease (0.95), or liver histology. Liver-related mortality appeared reduced when all trials were combined (0.50), but the effect vanished when only high-quality trials were considered (0.57, not significant). The authors noted the methodological quality was low (only 28.6% of trials were high quality) and concluded that the results 'question the beneficial effects' of milk thistle. There is no evidence that milk thistle halts real cirrhosisAdvanced liver disease in which long-term damage leaves the liver scarred, hardened, and failing. or hepatitis progression. PMID: 17943794

Lowering liver enzymes or viral levels in chronic hepatitis CEvidence type: RCTRandomized controlled trial - a high-reliability trial that randomly assigns participants to compare effects.

D Insufficient

None

A rigorous trial directly tested the belief that the milk-thistle compound silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent. helps the liver in hepatitis, and it did not. In a double-blind trial across 4 US centers (SyNCH) of 154 patients with chronic hepatitis C who had failed interferon therapy, silymarin was given at 420 mg or 700 mg a day (higher than customary doses) for 24 weeks. Only 2 people in each group reached a normal liver enzyme (ALT) level (placeboAn inert dummy treatment used as the comparison baseline. 3.8% vs silymarin 4.0% and 3.8%, no difference), the mean ALT change did not differ significantly from placebo (P=0.75), and there were no differences in hepatitis C virus (HCV RNA) levels or quality of life. Even higher-than-usual doses did not beat placebo. PMID: 22797645

Lowering liver enzymes (ALT/AST) in non-alcoholic fatty liver disease (NAFLDNon-alcoholic fatty liver disease - a common chronic condition of fat building up in the liver, unrelated to alcohol.)Evidence type: Meta-analysis

C Weak

Minimal

This is the one area where milk thistle shows any signal, but it stops at a surrogate marker. In a meta-analysisA statistical synthesis combining results of multiple studies into one conclusion. pooling 8 randomized trials in NAFLDNon-alcoholic fatty liver disease - a common chronic condition of fat building up in the liver, unrelated to alcohol. patients, silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent. lowered liver enzymes (ALT/AST) significantly more than placeboAn inert dummy treatment used as the comparison baseline., independent of weight loss. But the authors themselves cautioned about 'potential flaws related to the quality of the included studies' and stressed that 'further well-designed studies should be carried out to examine whether this reduction in transaminaseLiver-cell enzymes (ALT/AST); rising blood levels signal liver-cell damage. levels corresponds to histologic improvement.' A separate network meta-analysisA meta-analysis that ranks several treatments at once, including indirect comparisons. also found natural products like silymarin less effective than metabolic-target drugs such as obeticholic acid. So blood numbers come down somewhat, but whether that means real improvement of the fatty liver is unconfirmed. PMID: 33418491 · 33761646

Death-cap mushroom poisoning - intravenous silibininThe main active constituent of silymarin (also called silybin); an intravenous form is used to treat mushroom poisoning. (a hospital drug)Evidence type: Expert review

C Weak

Minimal

This is the one place a milk-thistle compound is genuinely used in medicine, but it is nothing like the pill on the shelf. Poisoning by amatoxinThe lethal toxin in death-cap and related mushrooms; it targets the liver and can cause liver failure.-containing mushrooms (such as the death cap) targets the liver and can progress to liver failure; there, hospitals use a purified intravenous form of silibininThe main active constituent of silymarin (also called silybin); an intravenous form is used to treat mushroom poisoning. (a semi-purified fraction of silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent.) together with N-acetylcysteine as adjunct supportive care. A European review presents combined silibinin + NAC therapy as recommended 'in the absence of an antidote,' noting that mortality is now under 10%. But this evidence is at the level of case reports and expert recommendation, not randomized trials, and it cannot isolate silibinin's own contribution. The key point: this is an intravenous drug used in the emergency room, not a supplement swallowed before drinking. PMID: 37949692

Evidence strength A Strong · B Moderate · C Weak · D Insufficient/refuted

Effect size Large → None

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Who benefits / who should be cautious

The statements in this section are translated directly from institutional sources (NIH-ODS, etc.), not our own interpretation. Consult a professional before use.

Caution

The belief that milk thistle changes the course of alcoholic or viral liver disease (cirrhosisAdvanced liver disease in which long-term damage leaves the liver scarred, hardened, and failing., hepatitis) is not supported by high-quality evidence. If you have real liver disease, proven medical care comes first, and milk thistle should not be used as a substitute for it. source↗

Original text

Our results question the beneficial effects of milk thistle for patients with alcoholic and/or hepatitis B or C virus liver diseases and highlight the lack of high-quality evidence to support this intervention.
Caution

In chronic hepatitis C, even higher-than-usual silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent. doses did not lower liver enzymes (ALT) more than placeboAn inert dummy treatment used as the comparison baseline.. It is not an ingredient that works by raising the dose, so if your liver numbers worry you, see a clinician rather than self-escalating. source↗

Original text

Higher than customary doses of silymarin did not significantly reduce serum ALT levels more than placebo in participants with chronic HCV infection unsuccessfully treated with interferon-based therapy.
Benefit

In non-alcoholic fatty liver disease, a meta-analysisA statistical synthesis combining results of multiple studies into one conclusion. found silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent. lowered liver enzymes (blood numbers) somewhat more than placeboAn inert dummy treatment used as the comparison baseline.. But the studies were low quality and it is unconfirmed whether that number change means real tissue improvement, so expectations should be modest. source↗

Original text

Silymarin seems to be effective in reducing transaminase levels in individuals with NAFLD. Despite the statistical benefits, we call attention to potential flaws related to the quality of the included studies. Further well-designed studies should be carried out to examine whether this reduction in transaminase levels corresponds to histologic improvement.

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Form & dosage evidence

Trial doses by effect

Chronic hepatitis C trial dose (the high dose that showed no effect): Silymarin 420 mg or 700 mg, three times a day for 24 weeks (SyNCH trial, no difference vs placebo) [22797645]

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Balanced conclusion

Milk thistle (silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent.) has weak evidence for actual liver disease relative to its reputation as a 'liver supplement.' A CochraneAn international network that rigorously reviews and synthesizes evidence. review found no significant effect on mortality, complications, or liver tissue in alcoholic and viral liver disease, and a rigorous US trial found that even high doses did not lower hepatitis C liver enzymes more than placeboAn inert dummy treatment used as the comparison baseline.. Even in non-alcoholic fatty liver disease, the one place with a signal, liver enzymes (blood numbers) come down somewhat, but whether that means real tissue improvement is unconfirmed and the studies are low quality. The one genuine medical use of a milk-thistle compound is intravenous silibininThe main active constituent of silymarin (also called silybin); an intravenous form is used to treat mushroom poisoning. given in hospitals for death-cap mushroom poisoning, a purified emergency drug, not the supplement swallowed around drinking. Silymarin has no special known toxicity (in Cochrane, adverse events resembled placebo), but as a member of the daisy family it warrants caution in allergy-prone people. In short, the belief that a milk-thistle supplement for drinking or liver health protects the liver is weakly grounded; if your liver numbers worry you, managing the cause and seeing a clinician come before a supplement.

Apply - Get it from food

Silymarin, the active compound of milk thistle, is extracted from the seeds of the milk thistle plant (Silybum marianum) and is not an ordinary food. Trusted government and peer-reviewed food-composition databases including USDA FoodData Central therefore do not list a silymarin content per food as a standard nutrient (this means the content values are not recorded in trusted databases, not that specific foods lack it). We therefore do not present a 'get it from food' table; it is consumed only as a seed-extract supplement.

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Sources

Each source shows its one-line summary and key summary up front. Expand the collapsed section to read the original abstract. Every citation is verified by re-resolving through the API.

PMID 17943794 Milk thistle for alcoholic and/or hepatitis B or C virus liver diseases Systematic review (Cochrane) · Cochrane Database Syst Rev, 2007 18 RCTRandomized controlled trial - a high-reliability trial that randomly assigns participants to compare effects.s, 1,088 patients - milk thistle showed no significant effect on mortality (RR 0.78), complications (0.95), or liver histology; the liver-death effect vanished in high-quality trials (0.57 NS). 'Questions the beneficial effects.'

Key summary

A CochraneAn international network that rigorously reviews and synthesizes evidence. systematic review of milk thistle in alcoholic and hepatitis B/C liver disease. It pooled 18 randomized trials and 1,088 patients, but methodological quality was low (only 28.6% of trials reported high-quality characteristics). Versus placeboAn inert dummy treatment used as the comparison baseline. or no intervention, milk thistle had no significant effect on mortality (relative risk 0.78, 95% CI 0.53-1.15), complications of liver disease (0.95, 0.83-1.09), or liver histology. Liver-related mortality fell significantly when all trials were combined (0.50, 0.29-0.88) but not in high-quality trials (0.57, 0.28-1.19). Adverse-event risk did not differ from placebo (0.83). The authors questioned the beneficial effects of milk thistle and stressed the lack of high-quality evidence.

Show original abstract

BACKGROUND: Alcohol and hepatotoxic viruses cause the majority of liver diseases. Randomised clinical trials have assessed whether extracts of milk thistle, Silybum marianum (L) Gaertneri, have any effect in patients with alcoholic and/or hepatitis B or C virus liver diseases. OBJECTIVES: To assess the beneficial and harmful effects of milk thistle or milk thistle constituents versus placebo or no intervention in patients with alcoholic liver disease and/or viral liver diseases (hepatitis B and hepatitis C). SEARCH STRATEGY: The Cochrane Hepato-Biliary Group Controlled Trials Register, The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, and full text searches were combined (July 2007). Manufacturers and researchers in the field were contacted. SELECTION CRITERIA: Only randomised clinical trials in patients with alcoholic and/or hepatitis B or C virus liver diseases (acute and chronic) were included. Interventions encompassed milk thistle at any dose or duration versus placebo or no intervention. The trials could be double blind, single blind, or unblinded. The trials could be unpublished or published and no language limitations were applied. DATA COLLECTION AND ANALYSIS: The primary outcome measure was mortality. Binary outcomes are reported as relative risks (RR) with 95% confidence interval (CI). Subgroup analyses were performed with regard to methodological quality. MAIN RESULTS: Eighteen randomised clinical trials assessed milk thistle in 1088 patients with alcoholic and/or hepatitis B or C virus liver diseases. The methodological quality was low: only 28.6% of the trials reported high methodological quality characteristics. Milk thistle versus placebo or no intervention had no significant effect on mortality (RR 0.78, 95% CI 0.53 to 1.15), complications of liver disease (RR 0.95, 95% CI 0.83 to 1.09), or liver histology. Liver-related mortality was significantly reduced by milk thistle in all trials (RR 0.50, 95% CI 0.29 to 0.88), but not in high-quality trials (RR 0.57, 95% CI 0.28 to 1.19). Milk thistle was not associated with a significantly increased risk of adverse events (RR 0.83, 95% CI 0.46 to 1.50). AUTHORS' CONCLUSIONS: Our results question the beneficial effects of milk thistle for patients with alcoholic and/or hepatitis B or C virus liver diseases and highlight the lack of high-quality evidence to support this intervention. Adequately conducted and reported randomised clinical trials on milk thistle versus placebo are needed. ※ The abstract text as collected and stored via the API by the pipeline. The key summary is written based solely on this text.

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PMID 22797645 Effect of silymarin (milk thistle) on liver disease in patients with chronic hepatitis C unsuccessfully treated with interferon therapy: a randomized controlled trial Randomized controlled trial (SyNCH) · JAMA, 2012 154 people, double-blind - silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent. 420 and 700 mg/day (high dose) did not lower ALT more than placeboAn inert dummy treatment used as the comparison baseline. at 24 weeks (P=0.75); no difference in HCV RNA or quality of life.

Key summary

A double-blind, placeboAn inert dummy treatment used as the comparison baseline.-controlled trial at 4 US centers in 154 patients with chronic hepatitis C who had failed interferon therapy. Silymarin 420 mg, 700 mg, or placebo was given three times a day for 24 weeks (higher than customary doses). Only 2 people per group reached the primary endpoint of a normalized ALT (placebo 3.8%, 420 mg 4.0%, 700 mg 3.8%, P>=0.99), and the mean ALT decline did not differ significantly across groups (P=0.75). There were no differences in hepatitis C virus (HCV RNA) levels (P=0.54) or quality of life, and adverse events resembled placebo. The authors concluded that even higher-than-customary silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent. doses did not lower ALT significantly more than placebo.

Show original abstract

CONTEXT: The botanical product silymarin, an extract of milk thistle, is commonly used by patients to treat chronic liver disease, despite scant and conflicting evidence of its efficacy. OBJECTIVE: To determine the effect of silymarin on liver disease activity in patients with chronic hepatitis C virus (HCV) infection unsuccessfully treated with interferon-based therapy. DESIGN, SETTING, AND PARTICIPANTS: Multicenter, double-blind, placebo-controlled trial conducted at 4 medical centers in the United States. Participants included 154 persons with chronic HCV infection and serum alanine aminotransferase (ALT) levels of 65 U/L or greater who were previously unsuccessfully treated with interferon-based therapy. Enrollment began in May 2008 and was completed in May 2010, with the last follow-up visit completed in March 2011. INTERVENTION: Participants were randomly assigned to receive 420-mg silymarin, 700-mg silymarin, or matching placebo administered 3 times per day for 24 weeks. MAIN OUTCOME MEASURES: The primary outcome measure was serum ALT level of 45 U/L or less (considered within the normal range) or less than 65 U/L, provided this was at least a 50% decline from baseline values. Secondary outcomes included changes in ALT levels, HCV RNA levels, and quality-of-life measures. RESULTS: After 24 weeks of treatment, only 2 participants in each treatment group (P >/= .99) met the primary outcome measure (3.8% [95% CI, 0.5% to 13.2%] for placebo, 4.0% [95% CI, 0.5% to 13.7%] for 420-mg silymarin, and 3.8% [95% CI, 0.5% to 13.2%] for 700-mg silymarin). The mean decline in serum ALT activity at the end of treatment did not differ significantly (P = .75) across the 3 treatment groups (mean decline, -4.3 [95% CI, -17.3 to 8.7] U/L for placebo, -14.4 [95% CI, -41.6 to 12.7] U/L for 420-mg silymarin, -11.3 [95% CI, -27.9 to 5.4] U/L for 700-mg silymarin); there likewise were no significant differences in HCV RNA levels (mean change, 0.07 [95% CI, -0.05 to 0.18] log10 IU/mL for placebo, -0.03 [95% CI, -0.18 to 0.12] log10 IU/mL for 420-mg silymarin, 0.04 [95% CI, -0.08 to 0.16] log10 IU/mL for 700-mg silymarin; P = .54) or quality-of-life measures. The adverse event profile of silymarin was comparable with that of placebo. CONCLUSION: Higher than customary doses of silymarin did not significantly reduce serum ALT levels more than placebo in participants with chronic HCV infection unsuccessfully treated with interferon-based therapy. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00680342. ※ The abstract text as collected and stored via the API by the pipeline. The key summary is written based solely on this text.

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PMID 33418491 Impact of Silymarin in individuals with nonalcoholic fatty liver disease: A systematic review and meta-analysis Systematic review and meta-analysis · Nutrition, 2021 8 RCTRandomized controlled trial - a high-reliability trial that randomly assigns participants to compare effects.s - silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent. lowered NAFLDNon-alcoholic fatty liver disease - a common chronic condition of fat building up in the liver, unrelated to alcohol. liver enzymes (ALT/AST) significantly more than placeboAn inert dummy treatment used as the comparison baseline. (independent of weight). But the authors warn of 'quality flaws' and that histologic improvement is unconfirmed.

Key summary

A systematic review and meta-analysisA statistical synthesis combining results of multiple studies into one conclusion. of 8 randomized trials of silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent. in NAFLDNon-alcoholic fatty liver disease - a common chronic condition of fat building up in the liver, unrelated to alcohol.. The primary outcomes were mean changes in liver enzymes (ALT/AST); secondary outcomes were body mass index and liver histology. Silymarin lowered liver enzymes significantly more than placeboAn inert dummy treatment used as the comparison baseline., independent of weight loss. But the authors warned of potential flaws in the quality of the included studies and concluded that well-designed further studies are needed to see whether this enzyme reduction corresponds to actual histologic improvement. So there is a change in a surrogate marker (blood numbers), but its clinical meaning is undetermined.

Show original abstract

OBJECTIVES: Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease affecting a significant proportion of the general population. Recently, randomized clinical trials have been conducted examining the efficacy of silymarin in individuals with NAFLD, with conflicting results. The aim of this meta-analysis was to evaluate the efficacy of silymarin in the treatment of NAFLD by examining changes in liver biochemistry, body mass index, and liver histology. METHODS: We searched major electronic databases PubMed/MEDLINE, Embase, and the Cochrane Central Register of Controlled Trials, as well as gray-literature sources, up to June 2020 for randomized clinical trials examining the efficacy of treatment with silymarin in individuals with NAFLD compared to placebo. The primary outcomes were changes in the mean values of transaminases (alanine aminotransferase and aspartate aminotransferase). Secondary outcomes included changes in body mass index and liver histology. Quality analysis was performed with the risk-of-bias tool 2.0. We synthesized results using weighted mean differences for continuous outcomes, along with 95% confidence intervals. RESULTS: In the meta-analysis, eight randomized clinical trials were included. A cutoff level of 0.05 was considered to provide statistically significant results. Silymarin treatment led to a statistically significant greater reduction in the levels of transaminases compared to placebo, irrespective of weight loss. CONCLUSIONS: Silymarin seems to be effective in reducing transaminase levels in individuals with NAFLD. Despite the statistical benefits, we call attention to potential flaws related to the quality of the included studies. Further well-designed studies should be carried out to examine whether this reduction in transaminase levels corresponds to histologic improvement. ※ The abstract text as collected and stored via the API by the pipeline. The key summary is written based solely on this text.

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PMID 33761646 The efficacy of novel metabolic targeted agents and natural plant drugs for nonalcoholic fatty liver disease treatment: A PRISMA-compliant network meta-analysis of randomized controlled trials Network meta-analysis · Medicine (Baltimore), 2021 35 RCTRandomized controlled trial - a high-reliability trial that randomly assigns participants to compare effects.s - in NAFLDNon-alcoholic fatty liver disease - a common chronic condition of fat building up in the liver, unrelated to alcohol., metabolic-target drugs like obeticholic acid led on liver biopsy and enzyme improvement; natural products like silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent. were generally less effective.

Key summary

A network meta-analysisA meta-analysis that ranks several treatments at once, including indirect comparisons. ranking metabolic-target drugs and natural products as NAFLDNon-alcoholic fatty liver disease - a common chronic condition of fat building up in the liver, unrelated to alcohol. treatments (35 randomized trials). Obeticholic acid and elafibranor ranked highest for liver-biopsy improvement and enzyme (ALT/AST) reduction, while natural products such as silymarinA complex of compounds extracted from milk thistle (Silybum marianum) seeds; silibinin is its main active constituent., curcumin, and resveratrol ranked lower. The authors concluded that novel metabolic-target agents are generally more effective than natural products (though obeticholic acid raised LDLLow-density lipoprotein cholesterol - the so-called "bad" cholesterol. and had other harms). This frames the point that even where silymarin shows some signal in fatty liver, it does not outperform proven drugs.

Show original abstract

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a highly prevalent chronic liver disease characterized by excess accumulation of fat in hepatocytes. Because no drug has been approved for NAFLD treatment, this work analyzed the effects of agents resulting from 2 research hotspots, metabolic target agents, and natural plant drugs, on NAFLD with network meta-analysis. METHODS: Public databases were searched through August 14, 2020. Randomized controlled trials that compared obeticholic acid, elafibranor, cenicriviroc, selonsertib, curcumin, silymarin, and resveratrol to placebo were included. Liver pathology improvement, hepatic biochemical indicators, and lipid metabolism indicators were analyzed. RESULTS: Thirty-five studies were included in the meta-analysis. Obeticholic acid was found to significantly increase the frequency of liver biopsy improvement compared to placebo (OR: 2.10; 95% CI: 1.60, 2.77). The ranking results among the hepatic biochemical indicators showed that obeticholic acid (94.9%) and elafibranor (86.3%) have a relative advantage in reducing alanine aminotransferase (ALT) levels, and obeticholic acid also had an advantage (95.4%) in reducing aspartate aminotransferase (AST) levels. Considering lipid metabolic indicators, elafibranor (expSMD: 0.01; 95% CI: 0.00, 0.05; SUCRA: 100%), and obeticholic acid (expSMD: 0.48; 95% CI: 0.28,0.84; SUCRA: 75.6%) significantly reduced triglyceride (TG) levels compared with placebo; moreover, obeticholic acid, but not elafibranor, caused a serious increase in total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels and a decrease in high-density lipoprotein cholesterol (HDL-C) levels. CONCLUSIONS: Novel metabolic targeted agents generally have better effects than natural plant drugs, especially obeticholic acid, and elafibranor. However, obeticholic acid showed serious adverse effects such as increasing LDL-C levels and decreasing HDL-C levels. Curcumin showed potential advantages for NAFLD but lacked statistical significance. ※ The abstract text as collected and stored via the API by the pipeline. The key summary is written based solely on this text.

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PMID 37949692 Amatoxin-containing mushroom poisoning: An update Expert review · Rev Med Interne, 2024 Review of amatoxinThe lethal toxin in death-cap and related mushrooms; it targets the liver and can cause liver failure. mushroom poisoning - with 'no antidote,' combined silibininThe main active constituent of silymarin (also called silybin); an intravenous form is used to treat mushroom poisoning. + N-acetylcysteine is recommended therapy; an IV adjunct, not an oral supplement.

Key summary

An expert review of amatoxinThe lethal toxin in death-cap and related mushrooms; it targets the liver and can cause liver failure.-containing mushroom poisoning (death cap and others). Amanita phalloides causes over 90% of mushroom-related deaths, and alpha-amanitin targets the liver, causing severe hepatitis and possible liver failure requiring transplantation. With no specific antidote, early hospital care is central, comprising fluids, gastrointestinal decontamination, enhanced elimination, amatoxin-uptake inhibitors, and antioxidant therapy. The authors present combined silibininThe main active constituent of silymarin (also called silybin); an intravenous form is used to treat mushroom poisoning. and N-acetylcysteine as recommended therapy, noting mortality is now under 10% thanks to improved resuscitation. Silibinin is used in this setting, but as a hospital intravenous therapy, and the evidence is not from randomized trials.

Show original abstract

Amatoxin-containing mushroom poisoning occurs after consumption of certain mushroom species, of the genera Amanita, Lepiota and Galerina. Amanita phalloides is the most implicated species, responsible for over more than 90% of mushroom-related deaths. The alpha-amanitin is responsible for most of the observed effects. Symptoms are characterized by severe delayed gastrointestinal disorders (more than six hours after ingestion). The liver being the main target organ, outcome is marked by an often severe hepatitis which can evolve towards terminal liver failure, justifying orthotopic liver transplantation. Acute renal failure is common. Diagnosis of amatoxin-containing mushroom poisoning is based primarily on clinical data; it can be biologically confirmed using detection of amatoxins, especially from urine samples. In the absence of an antidote, early hospital management is essential. It is based on supportive care (early compensation of hydroelectrolytic losses), gastrointestinal digestive decontamination, elimination enhancement, amatoxin uptake inhibitors and antioxidant therapy. Combined therapy associating silibinin and N-acetylcysteine is recommended. Prognosis of this severe poisoning has greatly benefited from improved resuscitation techniques. Mortality is currently less than 10%. In the event of a suspected or confirmed case, referral to a Poison Control Center is warranted in order to establish the diagnosis and guide the medical management of patients in an early and appropriate way. ※ The abstract text as collected and stored via the API by the pipeline. The key summary is written based solely on this text.

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Revision history

The full history of when and how this ingredient's evidence changed (git commits = proof of trust).

2026-07-13 First edition from real PubMed data - four milk thistle (silymarin) assessments ('good for the liver' belief vs the evidence). (1) Death/complications in alcoholic and viral liver disease D/none/meta (Cochrane Rambaldi 17943794: 18 RCTs, 1088 patients; mortality RR 0.78, complications 0.95, histology null; liver-death 0.50 overall but 0.57 NS in high-quality trials; 'questions the beneficial effects'). (2) Chronic hepatitis C enzymes/virus D/none/rct (SyNCH Fried 22797645 JAMA: 154 people; even high 420/700 mg silymarin did not beat placebo on ALT P=0.75, HCV RNA, QoL). (3) NAFLD enzyme reduction C/minimal/meta (Kalopitas 33418491: 8 RCTs, significant ALT/AST drop but 'quality flaws' + surrogate, histology unconfirmed; network meta Zhou 33761646: natural products < metabolic-target drugs). (4) Death-cap mushroom poisoning IV silibinin C/minimal/review (Caré 37949692: silibinin + NAC recommended but adjunct 'with no antidote,' not RCT, hospital IV not oral supplement). Key: the OTC pill has weak evidence for real liver disease; NAFLD shows only a surrogate signal; the one genuine medical use is purified IV silibinin in emergencies. No authoritative openFDA label (oral milk thistle is a supplement), so guidance grounded in Rambaldi, Fried, Kalopitas verbatim. Diet absent (silymarin is a milk-thistle seed extract, not in USDA and not an ordinary food). Reused category `botanical` and evidence_type `review`. Avoided banned words in display text. Glossary tooltips (silymarin, silibinin, cirrhosis, transaminase, NAFLD, amatoxin). Citation integrity, compliance, i18n, and dash/table conventions verified.

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