Home > 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 the 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 ultimately 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, 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:
Although many of these studies have produced encouraging results, none of the findings have been replicated in human clinical trials.
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 has been shown to stimulate phase II detoxification pathways in mice. Administration of silymarin (100 or 200 mg /kg body weight/day) to SENCAR mice for 3 days significantly increased glutathione S-transferase activity in the liver (P < .01-.001), lung (P < .05-.01), stomach (P < .05), small bowel (P < .01), and skin (P < .01). This effect appeared to be dose-dependent. Administration of silymarin to rats challenged with a toxin (50 mg/kg body weight) resulted in higher levels of glutathione in liver cells, decreased levels of oxidative stress (measured by malondialdehyde concentrations), and less elevated liver function tests (measured by levels of aspartate aminotransferase [AST] and alanine aminotransferase [ALT]). 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 synthesis of DNA.[35,36,37,38,39,40] Silymarin has been shown to mitigate oxidative stress in cells treated with pro-oxidant compounds.
A number of laboratory studies have investigated the effect of silymarin or silybin on the efficacy and toxicity of chemotherapy agents or have measured their direct cytotoxic activity. In an investigation of the effect of a variety of flavonoids on the formation of DNA damage, silymarin did not induce DNA damage in colon (Caco-2) cells, hepatoma (HepG2) cells, and human lymphocytes. At higher concentrations of silymarin (400-1,000 μmol/L) DNA damage was induced in an epithelial cell line (HeLa cells). At higher concentrations (1,000 μmol/L) DNA damage was observed in human lymphocytes. Cell growth was inhibited as the flavonoid concentration was increased in human lymphocytes and HeLa cells. Only at very high concentrations was cell viability affected by silymarin in HepG2 cells. Although this study demonstrated that the flavonolignans of Silybum marianum (L.) are capable of inhibiting cellular proliferation and inducing DNA strand breaks, the results were obtained at very high concentrations that may be difficult to achieve in humans. This study also showed that silymarin does not stimulate cell growth in the HeLa, Burkitt lymphoma, and human hepatoma cell lines.
Silymarin has also been investigated as a possible adjunctive agent in mitigating some of the toxicity associated with chemotherapy agents. Silybin and silychristin exerted a protective effect on monkey kidney cells exposed to vincristine and especially cisplatin chemotherapy. Silybin (200 mg/kg body weight) administration with cisplatin in rats resulted in statistically significant reductions in measures of kidney toxicity. Significant decreases in weight loss, faster recovery of urinary osmolality measures, and depressions in the increase in activity of urinary alanine aminopeptidase ([AAP], a marker of kidney toxicity) were observed. Silybin had no effect on magnesium excretion or glomerular function. Silybin (2 g /kg body weight) administration in rats receiving cisplatin prevented reductions in creatinine clearance, increases in urea plasma levels, and large increases in urinary AAP. No effect on magnesium excretion was observed. Silybin did not interfere with the antineoplastic effects of cisplatin or ifosfamide in germ cell tumors. In experiments with ovarian and breast cancer cell lines, silybin potentiated the effect of cisplatin and doxorubicin. IdB 1,016, a form of silybin bound to a phospholipid complex, was found to enhance the activity of cisplatin against A2780 ovarian cancer cells but had no effect on its own. Silybin increased the chemosensitivity of DU 145 prostate cancer cells resistant to chemotherapy.
Studies have also investigated the effect of silymarin on tumor initiation and promotion. Silymarin appears to have a chemopreventive effect through perturbations in the cell cycle, altering cell signaling that induces cellular proliferation, affecting angiogenesis, or through its anti-inflammatory properties.[1,7,13,19,46] These findings have been supported in human prostate, breast, ectocervical, ovarian, hepatic, leukemia, and epidermoid cell lines.[4,7,9,10,15,47] An investigation of the effect of silymarin on ultraviolet B radiation-induced nonmelanoma skin cancer in mice found that silymarin treatment significantly reduced tumor incidence (P < .003), tumor multiplicity (P < .0001), and tumor volume (P < .0001). These findings suggest that silymarin plays a prominent role in the reduction of cancer cells and in preventing the formation of cancer cells. A number of studies have investigated the mechanism through which silymarin may affect tumor promotion in mouse skin tumor models. Studies have found that silymarin reduces transcription of markers of tumor promotion and activity, inhibits transcription of tumor promoters, interferes with cell signaling, inhibits inflammatory actions,[19,22] and modulates cell-cycle regulation.
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.
In prostate cancer cell lines, silybin has been shown to inhibit growth factors and stimulate cell growth,[1,2,3,5] promote cell cycle arrest,[1,4] and inhibit antiapoptotic activity. In rats with azoxymethane -induced colon cancer, dietary silymarin resulted in a reduction in the incidence and multiplicity of adenocarcinoma of the colon in a dose-dependent manner.[25,26] Dietary silymarin had no effect on small intestinal adenocarcinoma, but exerted a preventive effect in mice with N-butyl-N-(4-hydroxybutyl) nitrosamine -induced bladder cancer  and in F344 rats with 4-nitroquinoline 1-oxide -induced cancer of the tongue. Dietary silybin administered to nude mice with prostate carcinoma increased production of insulin -like growth factor-binding protein-3 in the plasma of mice and significantly inhibited tumor volume (P < .05). Silibinin administered twice daily reduced the growth of colorectal tumor xenografts in mice for a period of 6 weeks.[52,53]
Several small studies have investigated silymarin for its effects on treatment related toxicity or for its direct treatment of cancer.
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 following 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 postradical 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.
In a nonrandomized observational trial of 101 women with breast cancer who had undergone breast-conserving surgery followed by radiation therapy (RT) 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 (SOG), 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 silymarin-based cream (45 vs. 29 days [SOC], P < .0001). Only 9.8% of patients using silymarin-based cream showed grade 2 toxicity in week 5 of RT, compared with 52% in the SOC group. At the end of RT, 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 only in 2% of women in the silymarin-based group and in 28% of women in the SOC group.
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/day 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 3 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.
Most clinical trials of milk thistle have been conducted in patients with either hepatitis or cirrhosis. Other studies have investigated milk thistle in patients with hyperlipidemia, diabetes, and Amanita phalloides (Fr.) mushroom poisoning. Ten randomized trials [1,5,6,7,8,9,10,11,12,13] 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 B, one clinical trial found silymarin (140 mg daily for 3-4 weeks) 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 daily) 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 herbals, 21% admitted past use, and 23% were using herbals at enrollment. Silymarin constituted 72% of the 60 herbals used at enrollment. Users had significantly fewer symptoms and a better QOL than 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 of the use of herbals for the treatment of chronic liver diseases, most treatment trials have suffered from poor scientific design, uncertainty of 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 the 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 are unable to 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/day 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 the 10 mg/kg, 15 mg/kg, and 20 mg/kg doses of silybinin. 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-week treatment with 560 mg/day of silymarin resulted in reductions of serum AST, ALT, 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 silybinin 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 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.
Current Clinical Trials
Check the list of NCI-supported cancer clinical trials for integrative, alternative, and complementary therapies clinical trials on milk thistle and silymarin that are actively enrolling patients.
General information about clinical trials is also available from the NCI website.
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 recent 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 within the recommended doses. Rare cases of milk thistle having 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 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 body weight. Rats and dogs have received silymarin at doses of 50 to 2,500 mg/kg 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 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 to date. 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).
Board members review recently published articles each month to determine whether an article should:
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:
Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
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.
Permission to Use This Summary
PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as "NCI's PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary]."
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]
Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.
The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.
More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website's Email Us.
Last Revised: 2016-07-20
Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated.
Addiction is treated by our Behavioral Health Doctors.
4 Medical Blvd,
Hattiesburg, MS 39402
27 B South 6th Street
Bay Springs, MS 39422
Covington County Hospital
701 S. Holly Ave
Collins, MS 39428
CONNECT WITH FORREST HEALTH
Notice of Privacy Practices · PUBLIC RECORDS REQUEST · FINANCIAL ASSISTANCE · NON-DISCRIMINATION NOTICE
REQUEST FROM LAW ENFORCEMENT FOR RELEASE OF PROTECTED HEALTH INFORMATION 6051 US HIGHWAY 49, HATTIESBURG MS 39401 · 601-288-7000 · © FORREST HEALTH · ALL RIGHTS RESERVED ·