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Home > Health Library > Milk Thistle (PDQ®): Integrative, alternative, and complementary therapies - Health Professional Information [NCI]
This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
This cancer information summary provides an overview of the use of milk thistle as a treatment and adjunct agent for people with cancer.
The summary includes a brief history of milk thistle, a review of the laboratory studies and clinical trials, and a description of adverse effects associated with milk thistle use.
This summary contains the following key information:
Many of the medical and scientific terms used in this summary are hypertext linked (at first use in each section) to the NCI Dictionary of Cancer Terms, which is oriented toward nonexperts. When a linked term is clicked, a definition will appear in a separate window.
Reference citations in some PDQ cancer information summaries may include links to external websites that are operated by individuals or organizations for the purpose of marketing or advocating the use of specific treatments or products. These reference citations are included for informational purposes only. Their inclusion should not be viewed as an endorsement of the content of the websites, or of any treatment or product, by the PDQ Integrative, Alternative, and Complementary Therapies Editorial Board or the National Cancer Institute.
The botanical name for milk thistle is Silybum marianum (L.) Gaertn. Milk thistle is also referred to as holy thistle, Marian thistle, Mary thistle, Our Lady's thistle, St. Mary thistle, wild artichoke, Mariendistel (German), and Chardon-Marie (French). The plant is indigenous to Europe but can also be found in the United States and South America. Traditionally, the leaves have been used in salads, and the fruit of the flower has been roasted as a coffee substitute. The seed-like fruits (achenes) of milk thistle are the medicinal parts of the plant. The active constituent of milk thistle is silymarin, which is a complex mixture of flavonoids and flavonoid derivatives, the flavonolignans. The major constituents of silymarin are the three diastereomeric pairs, silybins A and B (also called silibinin), isosilybins A and B, silychristin, isosilychristin, and silydianin.[2,3] Most supplements are standardized according to their silybin content. Special formulations of silymarin and/or the silybins have been developed to enhance their bioavailability by conjugation with phosphatidylcholine. Because of the lipophilic nature of its active constituents, milk thistle is usually administered as an extract in capsule or tablet form rather than as an herbal tea. In Europe, silybin is administered intravenously as the only effective antidote for Amanita phalloides (Fr.). Humans exposed to this mushroom toxin develop serious liver failure that progresses to death.
Several companies distribute milk thistle as a dietary supplement. In the United States, dietary supplements are regulated as foods, not drugs. Therefore, premarket evaluation and approval by the U.S. Food and Drug Administration (FDA) are not required unless specific disease prevention or treatment claims are made. Because dietary supplements are not formally reviewed for manufacturing consistency, ingredients may vary considerably from lot to lot; in addition, there is no guarantee that ingredients identified on product labels are present at all or are present in the specified amounts. The FDA has not approved the use of milk thistle as a treatment for cancer patients or patients with any other medical condition.
Despite milk thistle's long history of being used to treat liver and biliary complaints, it was not until 1968 that silymarin was isolated from the seeds of the plant, and it was proposed that silymarin might be the active ingredient. Researchers have investigated the role that silibinin may play in the treatment of hepatitis and cirrhosis. Most studies have investigated the isolated compound silymarin or its most active isomer silybin, rather than the herbal plant in its whole form.
Silymarin is most well known for its purported effects on the liver. In laboratory studies, silymarin has been found to stabilize cell membranes, thus preventing toxic chemicals from entering the cell.[4,6,7,8] Laboratory studies have also demonstrated that silymarin stimulates synthesis and activity of enzymes responsible for detoxification pathways.[7,8,9,10,11,12,13,14,15,16,17,18] Specifically, silymarin has been shown to stimulate the glutathione S-transferase pathway and alter the intracellular concentration of glutathione (a potent antioxidant). Silymarin has also been shown to neutralize a wide range of free radicals. Reports that associate the flavonolignans with potential estrogenic effect (e.g., via mediation of the estrogen receptor) are sparse and currently not supported by in vitro or in vivo experimental evidence.
Laboratory experiments conducted using cancer cell lines have suggested that silibinin enhances the efficacy of cisplatin and doxorubicin against ovarian and breast cancer cells. Silybin appears to have direct anticancer effects against prostate, breast, and ectocervical tumor cells. Silybin may also affect the cell cycle in cancer cells by slowing down cell growth, as demonstrated with prostate cancer cell lines. Laboratory studies using leukemia cell lines found that silybin did not stimulate growth of leukemia cells.
Most clinical trials have investigated silymarin's effectiveness in the treatment of patients with hepatitis, cirrhosis, or biliary disorders.[24,25,26,27,28,29,30,31,32,33] These studies have employed a wide range of doses (120–560 mg /day) and have yielded conflicting results.[34,35] The most commonly reported adverse effects are a mild laxative effect and gastrointestinal upset.
Milk thistle has been used for more than 2,000 years, primarily as a treatment for liver dysfunction. The oldest reported use of milk thistle was by Dioscorides (A.D. 40–90), who recommended the herb as a treatment for serpent bites. Pliny the Elder (A.D. 23–79) reported that the juice of the plant mixed with honey is indicated for "carrying off bile."[1,2] In the Middle Ages, milk thistle was revered as an antidote for liver toxins.[1,2] The British herbalist Culpepper reported milk thistle to be effective for relieving obstructions of the liver.[1,2] In 1898, eclectic physicians Felter and Lloyd stated the herb was good for congestion of the liver, spleen, and kidney.[1,2] Native Americans use milk thistle to treat boils and other skin diseases. Homeopathic practitioners use preparations from the seeds to treat jaundice, gallstones, peritonitis, hemorrhage, bronchitis, and varicose veins. The German Commission E recommends milk thistle use for dyspeptic complaints, toxin-induced liver damage, hepatic cirrhosis, and as a supportive therapy for chronic inflammatory liver conditions.
Research studies conducted in the laboratory have investigated the properties of silymarin or its isomer silybin using cell lines and animal models. Other substances in milk thistle have not been extensively studied.
Several research studies have investigated the effects of silymarin or silybin in a noncancer context. These studies have tested silymarin or silybin:
Silymarin or silybin has also been investigated in cancer models. The effects of silymarin and/or silybin have been investigated in prostate (DU 145, LNCaP, PC-3),[1,2,3,4,5,6]breast (MDA-MB 468, MCF-7),[7,8,9]hepatic (HepG2),[10,11] epidermoid (A431),colon (Caco-2),ovarian (OVCA 433, A2780),histiocytic lymphoma (U-937), and leukemia (HL-60) [15,16] cells. In animal tumor models, tongue cancer, skin cancer,[18,19,20,21,22,23]bladder cancer, and adenocarcinoma of the colon [25,26] and small intestine  have been investigated. These studies have tested the ability of silymarin or silibinin to:
Laboratory data suggest that silymarin and silybin protect the liver from damage induced by toxic chemicals. Animal studies have found that liver cells treated with silybin and then exposed to toxins do not incur cell damage or death at the same rate as liver cells that are not treated with silybin. This finding suggests that silybin can prevent toxins from entering the cell or effectively exports toxins out of the cell before damage ensues.[11,27,28,29,30,31] Alternatively, this may be related to the effect of silymarin on detoxification systems. In vitro data have shown silybin to stimulate and/or inhibit phase I detoxification pathways in silybin-treated human liver cells. However, this effect was found to be dose-dependent, and these levels are not physiologically attainable with the current manufacturer dose recommendations.[32,33]
Silymarin and silybin have also been found to accelerate cell regeneration in the liver through stimulation of precursors to DNA synthesis and enhancement of production of the cellular enzymes required for DNA synthesis.[34,35,36,37,38,39] Silymarin has been shown to mitigate oxidative stress in cells treated with pro-oxidant compounds.
While some reports exist about the estrogenic effects assigned to silybin and silybin-containing materials, the observed effects are moderate, and the molecular mechanisms are not yet understood. Some evidence exists about the positive impact of these milk thistle compounds on bone density in rats and mice that have undergone ovariectomy.
Silibinin inhibits prostate cancer cell–induced osteoclastogenesis, suggesting that silibinin may be useful clinically for the treatment of bone metastases. Silibinin targets prostate cancer cell–induced osteoclast differentiation and activity of murine macrophage cells.
Although many of these studies have produced encouraging results, none of the findings have been replicated in human clinical trials.
Several in vitro studies have explored anticancer effects of milk thistle extracts. Silybinin has been shown to inhibit cell proliferation by inducing cell cycle arrest at the G1 and G2-M transition in epidermal,[7,44,45] prostate, breast, and cervical  cancer cell lines. One study also demonstrated that growth of colon cancer cell lines was inhibited by silibinin, apparently through suppression of NF-kappa B. Finally, silymarin has also been shown to induce differentiation in a human leukemia cell line.
Other in vitro studies have demonstrated that components of milk thistle extract can enhance the effects of certain cytotoxic agents against various cancer types (i.e., etoposide against LN229 glioma cells, cisplatin against A2780 ovarian cancer cells [13,51] and MCF-7 breast cancer cells, and tumor necrosis factor alpha against DU145 prostate cancer cells ).
Several small studies have investigated silymarin for its direct treatment of cancer or for its effects on treatment-related toxicity.
A phase I study was designed to determine the maximum tolerated dose per day of silybin phosphatidylcholine (Siliphos) in patients with advanced hepatocellular carcinoma (HCC) and hepatic dysfunction. Three patients were enrolled in this single-institution trial. All patients who were enrolled consumed 2 g /d of the study agent in divided doses. Serum concentrations of silibinin and silibinin glucuronide increased within 1 to 3 weeks. In all three patients, liver function abnormalities and tumor marker alpha-fetoprotein progressed, but after day 56, the third patient showed some improvement in liver function abnormalities and inflammatory biomarkers. All three patients died within 23 to 69 days of enrolling in the trial, likely from hepatic failure, but it could not be ruled out that deaths were possibly caused by the study drug. This patient population may have been too ill to benefit from an intervention designed to improve liver function tests.
In a double-blind, placebo-controlled trial, 50 children who were undergoing treatment for acute lymphoblastic leukemia, and who had chemotherapy -related hepatotoxicity, were randomly assigned to receive silymarin or placebo for a 4-week period. Four weeks after completion of the intervention, the silymarin group had a significantly lower aspartate aminotransferase (AST) (P = .05) and a trend towards a significantly lower alanine aminotransferase (ALT) (P = .07). Fewer chemotherapy dose reductions were observed in the silymarin group compared with the placebo group; however, the difference was not significant. No adverse events were reported.
A randomized placebo-controlled study of 37 men, who had a status of post–radical prostatectomy, investigated whether a 6-month daily administration of a silymarin and selenium combination would alter basic clinical chemistry, oxidative stress markers, and improve the quality-of-life (QOL) score in men after radical prostatectomy. The 6-month daily administration of silymarin and selenium improved the QOL score, decreased low-density lipoproteins and total cholesterol, and increased serum selenium levels. The combination had no effect on blood antioxidant status and no influence on testosterone level. No adverse events were recorded. No improvement was found in the placebo group.
Another randomized placebo-controlled study of 30 patients with head and neck cancer investigated a 6-week course of silymarin for the prevention of radiation therapy –associated mucositis. Mucositis scores (World Health Organization, National Cancer Institute Common Toxicity Criteria) were significantly lower in the silymarin group. Delay in progression to mucositis was also observed.
In a nonrandomized observational trial of 101 women with breast cancer who had undergone breast-conserving surgery followed by radiation therapy with 50.4 Gy plus a boost of 9 Gy to 16 Gy, a silymarin-based cream (Leviaderm) was tested in 51 women compared with panthenol-containing cream, the standard of care (SOC), which was given interventionally if local skin lesions occurred and administered to 50 women. The acute skin reactions were classified according to the Radiation Therapy Oncology Group and visual analog scale scores. The median time to toxicity was prolonged significantly with the silymarin-based cream (45 vs. 29 days [SOC], P < .0001). Only 9.8% of patients using the silymarin-based cream showed grade 2 toxicity in week 5 of radiation therapy, compared with 52% in the SOC group. At the end of radiation therapy, 23.5% of the women in the silymarin-based study group developed no skin reactions compared with 2% of the women in the SOC group, while grade 3 toxicity occurred in only 2% of women in the silymarin-based group and in 28% of women in the SOC group.
Most clinical trials of milk thistle have been conducted in patients with either hepatitis or cirrhosis. Other studies have investigated the use of milk thistle in patients with hyperlipidemia, diabetes, and Amanita phalloides (Fr.) mushroom poisoning. Ten randomized trials [2,6,7,8,9,10,11,12,13,14] have been reported in patients with hepatitis or cirrhosis, and one randomized trial has reported the use of silymarin as a prophylaxis to iatrogenic hepatic toxicity.Endpoints for these trials have included serum levels of bilirubin and/or the liver enzymes AST and ALT, as higher levels are an indicator of liver inflammation, damage, or disease. The lowering of these serum levels is a sign of an improving condition. In patients with hepatitis A and hepatitis B, one clinical trial found silymarin (140 mg daily for 3–4 wk) resulting in lower levels of AST, ALT, and bilirubin by day 5, compared with a placebo group. In another randomized, placebo-controlled study of patients with viral hepatitis B, silymarin (210 mg/d) had no effect on course of disease or enzyme levels.
A randomized, controlled trial supported by the National Institute of Diabetes and Digestive and Kidney Diseases examined patients with chronic hepatitis C who had failed previous antiviral therapy. All patients had advanced chronic liver disease consisting of histologic evidence of either marked fibrosis or cirrhosis. The Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis trial used a half dose of pegylated interferon versus no treatment; the treatment was to be administered for 3.5 years. The aim was to reduce progression of chronic hepatitis C, particularly in the development of HCC. Among 1,145 study participants, 56% had never taken herbal products, 21% admitted past use, and 23% were using herbal products at enrollment. Silymarin constituted 72% of the 60 herbal products used at enrollment. Users had significantly fewer symptoms and a better QOL than did nonusers. In follow-up, silymarin use was associated with reduced progression of fibrosis to cirrhosis but without an impact on clinical outcome.
Although there are many reports on the use of herbals for the treatment of chronic liver diseases, most treatment trials have suffered from poor scientific design, uncertainty about the required dosage of herbals, and an insufficient number of study participants. A review of complementary and alternative medications (CAM) to treat liver diseases focused on classification, epidemiology, and the philosophy of CAM and reviewed the criteria needed to conduct a scientifically valid research study focusing on herbal products.
There has been skepticism regarding the evidence that silymarin has a direct impact on the hepatitis C virus (HCV)—some studies suggest that it does, but most studies cannot confirm these reports. However, at least two articles in major journals have suggested that silymarin or its congeners may inhibit HCV. In one report, investigators found that a standardized silymarin extract inhibited tumor necrosis factor -alpha in anti-CD3–stimulated human peripheral blood mononuclear cells and nuclear factor-kappa B –dependent transcription in human hepatoma Huh-7 cells. Silymarin also displayed prophylactic and therapeutic effects against HCV infection, and when combined with interferon-alpha, was more inhibitory of HCV replication than was interferon alone. This indicates that silymarin has anti-inflammatory and antiviral effects in patients with chronic hepatitis C.
In a case series /phase I study, patients with HCV were treated with intravenous silibinin with and without PEG-interferon and ribavirin. In the case series, 16 HCV nonresponder patients were administered intravenous silibinin in a dose of 10 mg/kg/d for 7 days. Subjects then began treatment with oral silibinin in combination with PEG-interferon and ribavirin for 12 weeks. At the end of the study period, all patients were positive for HCV RNA, but 5 of 13 completed patients had reductions in HCV RNA. Significance was not reported. In the same study, the authors presented results of a phase I study in which 20 patients were administered 5 mg/kg, 10 mg/kg, 15 mg/kg, or 20 mg/kg of silibinin for 14 days in combination with PEG-interferon and ribavirin (initiated on day 8). A significant drop in HCV RNA was observed on day 7 in patients administered silibinin doses of 10 mg/kg, 15 mg/kg, and 20 mg/kg. Further declines were observed in HCV RNA with administration of PEG-interferon and ribavirin. Except for mild gastroenteritis, intravenous silibinin monotherapy was well tolerated.
Patients in a phase I pharmacokinetics study for the evaluation of absorption characteristics and determination of effective doses received increasing oral doses of silymarin. A subsequent multicenter, double-blind, placebo-controlled trial, involving 154 patients with chronic HCV infection who had previously failed interferon-based treatment and had raised ALT levels, was performed. Patients were randomly assigned to receive 420 mg of silymarin, 700 mg of silymarin, or a matching placebo orally 3 times per day for 24 weeks, with the aim of reducing ALT levels to less than 40 U/L or less than 65 U/L if this was at least a 50% decline from the baseline level. In this study, silymarin given orally in higher-than-usual doses failed to significantly reduce serum ALT levels. No significant adverse effects were associated with silymarin. In one of the largest observational studies involving 2,637 patients with chronic liver disease, 8 weeks of treatment with 560 mg of silymarin per day resulted in reductions of serum AST, ALT, and gamma-glutamyltranspeptidase (GGT, a marker of bile duct disease), and a decrease in the frequency of palpable hepatomegaly.
Another published report describes the use of silibinin as the only effective antidote in patients with liver damage from Amanita phalloides (Fr.) poisoning. Patients were administered doses of 35 to 55 mg/kg of body weight, with no reports of adverse events. A retrospective review of the treatment for Amanita phalloides (Fr.) poisoning suggests that silymarin has been shown to be an effective drug in the treatment of this mushroom poisoning. The beneficial effect of silymarin on liver histology suggests it has a role in the prevention of hepatitis and/or HCC; however, no clinical trials in humans have investigated these uses of silymarin.
Silymarin was found to be beneficial as an adjunct to the iron chelator desferrioxamine in patients with transfusion -dependent beta-thalassemia major. In a study of 97 patients, significant decreases in markers of iron overload (serum ferritin, serum iron, hepcidin, and soluble transferring receptor) were observed in the patients who received silymarin as compared with those who received a placebo.
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Human studies of silymarin have shown minimal adverse effects in multiple large, blinded, placebo-controlled, randomized studies. Silymarin is well tolerated, with only rare reports of a mild laxative effect. Mild allergic reactions have been seen at high doses (>1,500 mg /day), although the details of these allergic reactions were not reported. A case report from Australia described a reaction to a milk thistle extract that included intermittent episodes of sweating, abdominal cramping, nausea, vomiting, diarrhea, and weakness. All symptoms resolved when the silymarin was discontinued. The authors suggested that the capsules were contaminated; the type of contamination was unknown.
According to the German Commission E, there are no reported side effects with milk thistle when the recommended doses are used. Rare cases of milk thistle producing a laxative effect have been reported. Human studies have reported stomach upset, heartburn, and transient headaches; however, none of these symptoms were attributed to supplementation with milk thistle, and supplementation was not discontinued. One human dosing study reported nausea, heartburn, and dyspepsia in patients treated with 160 mg/day, dyspepsia in patients treated with 240 mg/day, and postprandial nausea and meteorism in patients treated with 360 mg/day. None of these side effects were dose related.
Silymarin has been well tolerated in high doses. Silymarin has been used in pregnant women with intrahepatic cholestasis at doses of 560 mg/day for 16 days, with no toxicity to the patient or the fetus. The published data on silymarin use in children focuses on intravenous doses of 20 to 50 mg/kg of body weight for mushroom poisoning. Silymarin has also proved nontoxic in rats and mice when administered in doses as high as 5,000 mg/kg of body weight. Rats and dogs have received silymarin at doses of 50 to 2,500 mg/kg of body weight for a 12-month period. Investigations, including postmortem analyses, showed no evidence of toxicity.
It is not known whether milk thistle may reduce, enhance, or have no impact on the effectiveness of chemotherapy. In vitro studies show that silymarin decreases the components of the cytochrome P450 enzyme system, which is involved in the clearance of certain chemotherapy drugs. However, the dose at which inhibition is observed is high and not achieved with oral intake of silymarin. One study investigated the effects of silymarin on the pharmacokinetics of irinotecan. Oral administration of milk thistle (200 mg, a clinically relevant dose, 3 times per day) had no significant effects on the pharmacokinetics of irinotecan. The authors concluded that the recommended doses of milk thistle are too low to affect activity of CYP3A4 or UGT1A1 enzyme pathways.
Theoretically, milk thistle may also interact adversely with chemotherapy drugs that exert their cytotoxic effects through the generation of free radicals. Silymarin and its metabolite inhibit p-glycoprotein–mediated cellular efflux, leading to the potentiation of doxorubicin cytotoxicity. No trials have been performed to support or negate these theoretical considerations. No effects on indinavir and alcohol pharmacokinetics have been observed. Enhancement of the antiarrhythmic effects of amiodarone in rats has been observed.
To assist readers in evaluating the results of human studies of integrative, alternative, and complementary therapies for cancer, the strength of the evidence (i.e., the levels of evidence) associated with each type of treatment is provided whenever possible. To qualify for a level of evidence analysis, a study must:
Separate levels of evidence scores are assigned to qualifying human studies on the basis of statistical strength of the study design and scientific strength of the treatment outcomes (i.e., endpoints) measured. The resulting two scores are then combined to produce an overall score. A level of evidence score cannot be assigned to milk thistle because there has been insufficient clinical research done. For an explanation of the scores and additional information about levels of evidence analysis of CAM treatments for cancer, refer to Levels of Evidence for Human Studies of Integrative, Alternative, and Complementary Therapies.
Given the limited amount of human data, the use of milk thistle/silymarin as a treatment for cancer patients cannot be recommended outside the context of well-designed clinical trials.
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Editorial changes were made to this summary.
This summary is written and maintained by the PDQ Integrative, Alternative, and Complementary Therapies Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® - NCI's Comprehensive Cancer Database pages.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the use of milk thistle in the treatment of people with cancer. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Integrative, Alternative, and Complementary Therapies Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
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Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
The lead reviewers for Milk Thistle are:
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Levels of Evidence
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Integrative, Alternative, and Complementary Therapies Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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The preferred citation for this PDQ summary is:
PDQ® Integrative, Alternative, and Complementary Therapies Editorial Board. PDQ Milk Thistle. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: https://www.cancer.gov/about-cancer/treatment/cam/hp/milk-thistle-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389223]
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Last Revised: 2019-04-24
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