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[Big'r]

Milk thistle/ Silymarin/ Silybin

CONTENT
Milk thistle for liver protection
Milk thistle is very effective in treating amatoxin poisoning. It seems to decrease liver-related mortality in alcoholic and hepatitis B or C liver diseases.
Silybin+vitamin E+ phospholipids produces some therapeutic effects in patients with different forms of chronic liver damage.
Milk thistle does not affect viral load or improve liver histology in hepatitis B or C.
Milk thistle + the prostate
No "in vivo" human studies on the effect of milk thistle have been done/finished yet.
All reviews (4), in vitro studies (11), and rat/mouse studies (4) show a positive effect of milk thistle in preventing/treating prostate cancer.
Other studies
Silybin-beta-cyclodextrin causes a significant decrease in both glucose and triglyceride plasma levels.
"Normal" silybin shows no effect on fasting blood glucose.
Bioavailability + dosages
Liverman capsules are more effective than leganon and silymarin tablets.
Silipide reaches much higher bile and plasma silybin concentrations than silymarin.
Complexation with phosphatidylcholine in IdB 1016 greatly increases the oral bioavailability of silybin.
420 mg has therapeutic potential in alcoholic cirrhosis. 20-48 mg/kg/day is a promising antidote for acute mushroom poisoning.
Side effects
Only rare case reports of gastrointestinal disturbances and allergic skin rashes have been published.




MILK THISTLE FOR LIVER PROTECTION:

Treatment of amatoxin poisoning: 20-year retrospective analysis.
Amatoxin poisoning is ascribed to 35 amatoxin-containing species belonging to three genera: Amanita, Galerina, and Lepiota.
Clinical data from 2108 hospitalized amatoxin poisoning exposures as reported in the medical literature from North America and Europe over the last 20 years were compiled.
Chi-square statistical comparison of survivors and dead vs. treated individuals supported silybin, administered either as mono-chemotherapy or in drug combination and N-acetylcysteine as mono-chemotherapy as the most effective therapeutic modes (M405).

Milk Thistle for Alcoholic and/or Hepatitis B or C Liver Diseases-A Systematic Cochrane Hepato-Biliary Group Review with Meta-Analyses of Randomized Clinical Trials.
METHODS: Randomized clinical trials studying patients with alcoholic and/or hepatitis B or C liver diseases were included (December 2003). The randomized clinical trials were evaluated by components of methodological quality. RESULTS: Thirteen randomized clinical trials assessed MT in 915 patients with alcoholic and/or hepatitis B or C liver diseases.
MT versus placebo or no intervention for a median duration of 6 months had no significant effects on all-cause mortality (relative risk (RR) 0.78, 95% confidence interval (CI) 0.53-1.15), complications of liver disease, or liver histology. Liver-related mortality was significantly reduced by MT in all trials (RR 0.50, 95% CI 0.29-0.88 ), but not in high-quality trials (RR 0.57, 95% CI 0.28-1.19). MT was not associated with a significantly increased risk of adverse events (M407).

Silymarin treatment of viral hepatitis: a systematic review.
An exhaustive search strategy identified 148 papers that studied silymarin compounds in liver disease. Of these, four trials included patients with hepatitis C, one included hepatitis B patients, and two, unspecified chronic viral hepatitis. However, only one trial exclusively studied patients with hepatitis C, and none involved patients with only hepatitis B. Silymarin treatment resulted in a decrease in serum transaminases compared with baseline in four studies, and compared with placebo in only one study. There is no evidence that silymarin affects viral load or improves liver histology in hepatitis B or C (M409).

Milk thistle for the treatment of liver disease: a systematic review and meta-analysis.
We searched English and non-English reports through July 1999 using thirteen databases and reference lists, and contacting manufacturers and technical experts. Reviewers independently screened all reports to identify randomized placebo-controlled trials that evaluated milk thistle for the treatment of liver disease.
Fourteen trials met inclusion criteria. Four trials reported outcomes for mortality among 433 participants. The overall summary odds ratio for mortality in the milk thistle group compared with placebo was 0.8 (95% confidence interval [CI]: 0.5 to 1.5; P = 0.6).
Treatment with milk thistle appears to be safe and well tolerated. We found no reduction in mortality, in improvements in histology at liver biopsy, or in biochemical markers of liver function among patients with chronic liver disease (M415).

[Effects of a new pharmacological complex (silybin + vitamin-E + phospholipids) on some markers of the metabolic syndrome and of liver fibrosis in patients with hepatic steatosis. Preliminary study]
Eighty five patients were consecutively enrolled in the study and divided in 2 groups; the first group was represented by 59 patients affected by non alcoholic fatty liver disease (NAFLD), negative for other known causes of chronic liver damage (M/F= 39/20; median age and range: 44 years, 22-76, group A); the second group was represented by 26 patients (M/F=19/7; median age and range 51 years, 20-75, group B) with HCV-related chronic hepatitis associated to NAFLD.
This open preliminary study shows that the new compound silybin+vitamin E+ phospholipids is active, in vivo, and produces some therapeutic effects in patients with different forms of chronic liver damage. In particular, it improves insulin resistance and plasma levels of markers of liver fibrosis in patients in whom these parameters are particularly altered (M416).

Medicinal herbs for hepatitis C virus infection: a Cochrane hepatobiliary systematic review of randomized trials.
The databases of the Cochrane Collaboration, MEDLINE, EMBASE, and BIOSIS were searched combined with manual searches of five Chinese and one Japanese journals. We included randomized trials comparing medicinal herbs with placebo, no intervention, nonspecific treatment, other herbs, or interferon and/or ribavirin. Trials of herbs with or without other drug(s) were included.
Thirteen randomized trials (n = 818 ) evaluated 14 medicinal herbs. Four trials had adequate methodology. Compared with placebo, none of the herbs showed effects on HCV RNA or liver enzyme, except for silybin, which showed a significant reduction of serum AST and gamma-glutamyltranspeptidase levels in one trial (M417).

Silymarin: a review of its clinical properties in the management of hepatic disorders.Studies in patients with liver disease have shown that silymarin increases superoxide dismutase (SOD) activity of lymphocytes and erythrocytes, as well as the expression of SOD in lymphocytes. Silymarin has also been shown to increase patient serum levels of glutathione and glutathione peroxidase. Silybin 20 to 48 mg/kg/day has shown promise as a clinical antidote to acute Amanita (deathcap mushroom) poisoning. Primary efficacy data from 3 trials which examined the therapeutic potential of silymarin in patients with cirrhosis, and included patient survival as an end-point, demonstrated that silymarin had no significant beneficial effect on patient mortality. However, upon subanalysis, silymarin 420 mg/day had a significantly beneficial effect on patient survival rate (compared with patients receiving placebo) in 1 randomised, double-blind trial in patients with alcoholic cirrhosis. Silymarin 420 mg/day was also shown to improve indices of liver function [AST, ALT, gamma-glutamyl transferase and bilirubin] in patients with liver disease of various aetiology, including those exposed to toxic levels of toluene or xylene; however, it was largely ineffective in patients with viral hepatitis. Reports of adverse events while receiving silymarin therapy are rare. However, there have been accounts of nausea, epigastric discomfort, arthralgia, pruritus, headache and urticaria. Silymarin has also been reported to have possibly caused a mild laxative effect (M419).

Medicinal herbs for hepatitis C virus infection.
Searches were applied to The Controlled Trial Registers of The Cochrane Hepato-Biliary Group, The Cochrane Complementary Medicine Field, and The Cochrane Library as well as MEDLINE, EMBASE, BIOSIS, Chinese and Japanese databases. Five Chinese journals and one Japanese journal were handsearched. No language restriction was used. SELECTION CRITERIA: Randomised clinical trials comparing medicinal herbs (single herb or compound of herbs) versus placebo, no intervention, general non-specific treatment, other herbal medicine, or interferon and/or ribavirin treatment. Trials of medicinal herbs plus interferon and/or ribavirin versus interferon and/or ribavirin alone were also included. Trials could be double-blind, single-blind, or unblinded.
Ten randomised trials, including 517 patients with mainly chronic hepatitis C, evaluated ten different medicinal herbs versus various control interventions (four placebo, four interferon, two other herbs).
Compared with placebo in four trials, none of the medicinal herbs showed positive effects on clearance of serum HCV RNA or anti-HCV antibody or on serum liver enzymes, except one short-term trial in which a silybin preparation showed a significant effect on reducing serum aspartate aminotransferase and gamma-glutamyltranspeptidase activities (M420).

1 Interesting non-human study:

[Hepatoprotective effects of silymarin in androgenic-anabolic steroid-induced liver damage]
40 Male Wistar rats, divided into 4 groups of 10 rats each. Animals in the first experimental group (M), were subjected to progressive systematic forced swimming test, 5 days a week, during 8 weeks. Animals in this group were treated with AAS methandienone, 2 mg/kg BW/day, per os, before swimming, 5 d/w for 8 weeks. After swimming, animals were given three times more food than the laboratory animals of the same age and kind. Animals in the second group (M+S), were subjected to progressive forced swimming test, 5 d/w 8 weeks. Animals in this group were treated with methandienone equally as the experimental group M and received the same amount of food. Apart from that, they received silymarin 20 mg/kg BW/day. Animals in the third group (K), represented the control group, which was neither subjected to swimming test, nor treated with methandienone or silymarin. Animals in this group received the same amount of food as animals in groups M and M+S. Animals in the fourth group (C), also represented a control.
In cell nuclei of animals in the experimental group M, in the absence of silymarin effect, methandienone causes damages which induce regenerative processes and in this way increase high intensity activity. Silymarin significantly increases the glycogen density in hepatocytes. Increased activities of GDH are attributed to cell vitality. CONCLUSION: The present results show hepatoprotective effects of silymarin in androgenic-anabolic steroid induced liver damage (M403).

MILK THISTLE + THE PROSTATE:

11-2005 (pubmed search: milk thistle AND prostate --> 15 hits)
11-2005 (pubmed search: silybin AND prostate NOT milk NOT thistle --> 4 hits)

A cancer chemopreventive agent silibinin, targets mitogenic and survival signaling in prostate cancer.
We have observed that silibinin inhibits prostate tumor growth in animal models without any apparent signs of toxicity. At the same time, silibinin is also physiologically available in different organs of the body including plasma and prostate, which is generally required for the pharmacological dosing and translational mechanistic studies of the compound (M701).

Inhibition of telomerase activity and secretion of prostate specific antigen by silibinin in prostate cancer cells.
The down-regulation of PSA by silibinin and its counteraction on DHT effects indicate that this compound can interact with the expression of genes that are regulated through the androgen receptor (M702).

Cell signaling and regulators of cell cycle as molecular targets for prostate cancer prevention by dietary agents.
Prostate cancer (PCA) is the most common invasive malignancy and leading cause (after lung) of cancer deaths in males. Since PCA is initially androgen-dependent, strategies are targeted toward androgen depletion for its control. However, tumor re-growth mostly occurs following this modality, and is androgen-independent.
We focused our attention on silymarin, genistein, and epigallocatechin 3-gallate (EGCG), present in milk thistle, soy beans, and green tea, respectively.
Cell signaling and regulators of cell cycle are potential epigenetic molecular targets for prostate cancer prevention by dietary agents (M703).

Tissue distribution of silibinin, the major active constituent of silymarin, in mice and its association with enhancement of phase II enzymes: implications in cancer chemoprevention.SENCAR mice were starved for 24 h, orally fed with silibinin (50 mg/kg dose) and killed after 0.5, 1, 2, 3, 4 and 8 h.
Taken together, the results of the present study clearly demonstrate the bioavailability of and phase II enzyme induction by systemically administered silibinin in different tissues, including skin, where silymarin has been shown to be a strong cancer chemopreventive agent (M704).

OTHER STUDIES:

Silybin-beta-cyclodextrin in the treatment of patients with diabetes mellitus and alcoholic liver disease. Efficacy study of a new preparation of an anti-oxidant agent.
Sixty outpatients were enrolled in a three-centre, double blind, randomised, silybin-beta-cyclodextrin (IBI/S) vs placebo study. Forty-two (21 in the group IBI/S - 135 mg/d silybin per os - and 21 in the placebo group) concluded the 6-month treatment period.
Fasting blood glucose levels, which were similar at baseline in IBI/S group and in the placebo group (173.9 mg/dl and 177.1 mg/dl, respectively), decreased to 148.4 mg/dl (-14.7% vs baseline; p = 0.03) in the IBI/S group while they were virtually unchanged in the placebo group. The comparison between the groups at mo 6 (T6) also showed a significant reduction of glucose levels in the IBI/S group (p = 0.03). The same trend was observed in mean daily blood glucose levels, HbA1c and HOMA-IR, although differences were not significant. Basal and stimulated C-peptide values showed that only a few changes had occured in both groups. Such results indicate that insulin secretion was virtually unaffected, as confirmed also by the insulinemia data. Plasma triglycerides concentrations dropped from a baseline value of 186 mg/dl to 111 mg/dl (T6) in the IBI/S group, with significant differences at all instances with respect to baseline values. By contrast, triglycerides increased from 159 mg/dl at entry to 185 mg/dl (T6) in the placebo group. The difference between the groups at T6 was highly significant (p < 0.01). Total and HDL cholesterol as well as liver function tests did not change significantly during the study in both groups. MDA decreased significantly only in the group receiving IBI/S. No clinically relevant side effects were observed in either group. CONCLUSIONS: Oral administration silybin-beta-cyclodextrin in patients with T2DM and compensated chronic alcoholic liver disease causes a significant decrease in both glucose and triglyceride plasma levels. These effects may be due to the recovery of energy substrates, consistent with a reduced lipid peroxidation and an improved insulin activity (M418 ).

[Effects of silybin on red blood cell sorbitol and nerve conduction velocity in diabetic patients]
The effects of silybin on red blood cell (RBC) sorbitol and nerve conduction velocity in 14 non-insulin dependent diabetic patients (female 9, male 5; average age 58.2 years) were reported.
Silybin treatment had no effect on fasting blood glucose. In addition, silybin treatment slightly improved nerve conduction velocity, but statistically not significant. This report suggests that silybin may be a potent aldose reductase inhibitor, and valuable in the prophylaxis and treatment of diabetic complications (M421).

BIOAVAILABILITY + DOSAGES:

Comparative bioavailability of silibinin in healthy male volunteers.
Twenty-four healthy male Korean volunteers received each medicine at the silibinin dose of 120 mg in a 3 x 3 crossover study.
After an oral administration of Liverman capsule, the pharmacokinetic parameters of silibinin, such as AUC(0-12h) (5.59, 4.24 and 13.9 microg/ml x h for Legalon capsule, Silymarin tablet and Liverman capsule, respectively) and AUCinf (6.00, 4.63 and 15.1 microg/ml x h) were significantly greater, Cmax (1.33, 1.13 and 6.04 microg/ml) was significantly higher and tmax (1.83, 2.10 and 0.875 h) was significantly faster than those after Legalon capsule and Silymarin tablet. CONCLUSION: These results indicate that the absorption and the extent of relative oral bioavailability of silibinin after Liverman capsule were significantly faster and greater, respectively, than those after Legalon capsule and Silymarin tablet (M807).

Silymarin: a review of its clinical properties in the management of hepatic disorders.
Although silymarin has low oral absorption, oral dosages of 420 mg/day have shown some therapeutic potential, with good tolerability, in the treatment of alcoholic cirrhosis. Moreover, silybin 20 to 48 mg/kg/day has shown promise as an antidote for acute mushroom poisoning by Amanita phalloides; however, further studies paying attention to the amount of ingested mushroom and time elapsed before administration of treatment are needed to clarify its role in this indication. Studies in patients with the early onset of liver disease may demonstrate the liver regeneration properties that silymarin is promoted as possessing (M419).

Softgel capsule technology as an enhancer device for the absorption of natural principles in humans. A bioavailability cross-over randomised study on silybin.
An open, single dose, two-way, balanced cross-over study, was performed. The study was conducted on 12 healthy subjects (6 M and 6 F). 80 mg of silybin in a 1:2 complex with phosphatidylcholine was administered.
The mean values of both Cmax and AUC0-1 were increased when the patented soft gelatine capsule formulations were administered (i.e. Cmax more than 3-fold and AUC0-1 more than 2-fold) (M808 ).

Plasma concentrations of free and conjugated silybin after oral intake of a silybin-phosphatidylcholine complex (silipide) in healthy volunteers.
The plasma concentrations of free (unconjugated) and conjugated silybin after intake of a single oral dose of a lipophilic silybin-phospatidylcholine complex (silipide, 80 mg expressed as silybin equivalents) were evaluated in 12 healthy volunteers.
Free silybin concentrations reached a peak of 141 +/- 31 ng/ml (mean +/- SEM) at 2.4 hours after dosing and declined thereafter with a half-life of about 2 hours. Peak concentrations of conjugated silybin were greater (255 +/- 35 ng/ml) and occurred at a later time (about 3.8 hours). The elimination of conjugated drug tended to be slower than that of free drug. AUC values for conjugated sylibin were about three-fold greater than those of free drug. It is concluded that after oral intake of silipide, silybin undergoes extensive conversion to conjugated derivative(s) which are retained in the circulation at relatively large concentrations (M809).

Pharmacokinetics of silybin in bile following administration of silipide and silymarin in cholecystectomy patients.
The biliary excretion of silybin, the main active component of silymarin, was evaluated by using a specific HPLC method in 9 cholecystectomy patients with T-tube drainage following single oral doses of silipide (CAS 134499-06-2), a lipophilic silybin-phosphatidylcholine complex (IdB 1016), and of silymarin (120 mg, expressed as silybin equivalents). After intake of silipide, the concentration of silybin in bile reached a peak within 4 h and declined thereafter with a mean time of about 10 h. After administration of silymarin, biliary silybin concentrations were several-fold lower than those observed after intake of silipide.
The amount of silybin recovered in bile in free and conjugated form within 48 h accounted for 11% of the dose after silipide and for 3% of the dose after silymarin. Plasma silybin concentrations, determined in 3 subjects, were several-fold lower than those in bile after intake of silipide and mostly undetectable after intake of silymarin. These data indicate that the bioavailability of silybin is much greater after administration of silipide than after administration of silymarin (M810).

Pharmacokinetic studies on IdB 1016, a silybin- phosphatidylcholine complex, in healthy human subjects.
IdB 1016 is a complex of silybin (the main active component of silymarin) and phosphatidylcholine, which in animal models shows greater oral bioavailability.
Plasma silybin levels were determined after administration of single oral doses of IdB 1016 and silymarin (equivalent to 360 mg silybin) to 9 healthy volunteers. Although absorption was rapid with both preparations, the bioavailability of IdB 1016 was much greater than that of silymarin, as indicated by higher plasma silybin levels at all sampling times after intake of the complex. Regardless of the preparation used, the terminal half-life was relatively short (generally less than 4 h). In a subsequent study, 9 healthy volunteers received IdB 1016 (120 mg b.i.d., expressed as silybin equivalents) for 8 consecutive days. The plasma silybin level profiles and kinetic parameters on day 1 were similar to those determined on day 8.
Complexation with phosphatidylcholine in IdB 1016 greatly increases the oral bioavailability of silybin, probably by facilitating its passage across the gastrointestinal mucosa (M811).

SIDE EFFECTS:

Milk thistle.
Clinical studies are largely heterogeneous and contradictory. Aside from mild gastrointestinal distress and allergic reactions, side effects are rare, and serious toxicity rarely has been reported. In an oral form standardized to contain 70 to 80 percent silymarin, milk thistle appears to be safe for up to 41 months of use. Significant drug reactions have not been reported (M801).

Milk thistle for alcoholic and/or hepatitis B or C virus liver diseases.
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 (December 2003). 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.
Milk thistle was not associated with a significantly increased risk of adverse events (RR 0.83, 95% CI 0.46 to 1.50) (M802).

Silybin inactivates cytochromes P450 3A4 and 2C9 and inhibits major hepatic glucuronosyltransferases.
careful administration of silybin with drugs primarily cleared by P450s 3A4 or 2C9 is advised, since drug-drug interactions cannot be excluded (M803).

The use of alternative medicine in the treatment of hepatitis C.
Silymarin has a good safety record and only rare case reports of gastrointestinal disturbances and allergic skin rashes have been published (M805).

Preventive strategies in chronic liver disease: part I. Alcohol, vaccines, toxic medications and supplements, diet and exercise.
Many herbal remedies are potentially hepatotoxic, and only milk thistle can be used safely in patients who have chronic liver disease. Weight reduction and exercise can improve liver function in patients with fatty liver (M806).

And 1 possibly interesting mouse study:

Physiological responses of a natural antioxidant flavonoid mixture, silymarin, in BALB/c mice: III. Silymarin inhibits T-lymphocyte function at low doses but stimulates inflammatory processes at high doses.
Male BABL/c mice (6/group) were treated intraperitoneally once daily for five days with 0, 10, 50 or 250 mg/kg of silymarin. Silymarin exposure did not produce any signs of overt toxicity or any changes in relative organ weights.
The results indicate that in vivo parenteral exposure to silymarin results in suppression of T-lymphocyte function at low doses and stimulation of inflammatory processes at higher doses (M804).

REFERENCES:

M403)http://www.ncbi.nlm.nih.gov/entrez/q...919&query_hl=1
M405)http://www.ncbi.nlm.nih.gov/entrez/q...187&query_hl=1
M407)http://www.ncbi.nlm.nih.gov/entrez/q...916&query_hl=1
M409)http://www.ncbi.nlm.nih.gov/entrez/q...756&query_hl=1
M415)http://www.ncbi.nlm.nih.gov/entrez/q...501&query_hl=1
M416)http://www.ncbi.nlm.nih.gov/entrez/q...709&query_hl=1
M417)http://www.ncbi.nlm.nih.gov/entrez/q...784&query_hl=1
M418 )http://www.ncbi.nlm.nih.gov/entrez/q...659&query_hl=1
M419)http://www.ncbi.nlm.nih.gov/entrez/q...257&query_hl=1
M420)http://www.ncbi.nlm.nih.gov/entrez/q...177&query_hl=1
M421)http://www.ncbi.nlm.nih.gov/entrez/q...645&query_hl=1
M701)http://www.ncbi.nlm.nih.gov/entrez/q...849&query_hl=1
M702)http://www.ncbi.nlm.nih.gov/entrez/q...315&query_hl=1
M703)http://www.ncbi.nlm.nih.gov/entrez/q...941&query_hl=1
M704)http://carcin.oxfordjournals.org/cgi...ull/20/11/2101
M801)http://www.aafp.org/afp/20051001/1285.html
M802)http://www.ncbi.nlm.nih.gov/entrez/q...671&query_hl=1
M803)http://dmd.aspetjournals.org/cgi/content/full/32/6/587
M804)http://www.ncbi.nlm.nih.gov/entrez/q...278&query_hl=1
M805)http://www.ncbi.nlm.nih.gov/entrez/q...634&query_hl=1
M806)http://www.aafp.org/afp/20011101/1555.html
M807)http://www.ncbi.nlm.nih.gov/entrez/q...709&query_hl=1
M808 )http://www.ncbi.nlm.nih.gov/entrez/q...434&query_hl=1
M809)http://www.ncbi.nlm.nih.gov/entrez/q...377&query_hl=1
M810)http://www.ncbi.nlm.nih.gov/entrez/q...780&query_hl=1
M811)http://www.ncbi.nlm.nih.gov/entrez/q...770&query_hl=1

[MrJ]

Nice.

Als je je post edit dat de smileys uitstaan verplaats ik hem even naar de Leerzame Threads sectie.

[ECLIPSE]

CONCLUSION: The present results show hepatoprotective effects of silymarin in androgenic-anabolic steroid induced liver damage (M403).

ja leuk, maar heeft het ook invloed op de effectiviteit van de AAS, of welk ander medicijn dan ook for that matter.. ik denk dat daar de meesten hier geinterreseerd in zijn

[G21]

daarom ook altijd na de nakuur gebruiken..ivm het invloed hebben op aas en medicijnen..

goei post big'r!!!

[4CC]

BioDrugs 2001;15(7):465-89 Related Articles, Books, LinkOut


Silymarin: a review of its clinical properties in the management of hepatic disorders.

Wellington K, Jarvis B.

Adis International Limited, Auckland, New Zealand. demail@adis.co.nz

The mechanisms of action of silymarin involve different biochemical events, such as the stimulation of the synthetic rate of ribosomal RNA (rRNA) species through stimulation of polymerase I and rRNA transcription, protecting the cell membrane from radical-induced damage and blockage of the uptake of toxins such as alpha-amanitin. Studies in patients with liver disease have shown that silymarin increases superoxide dismutase (SOD) activity of lymphocytes and erythrocytes, as well as the expression of SOD in lymphocytes. Silymarin has also been shown to increase patient serum levels of glutathione and glutathione peroxidase. Silybin 20 to 48 mg/kg/day has shown promise as a clinical antidote to acute Amanita (deathcap mushroom) poisoning. Primary efficacy data from 3 trials which examined the therapeutic potential of silymarin in patients with cirrhosis, and included patient survival as an end-point, demonstrated that silymarin had no significant beneficial effect on patient mortality. However, upon subanalysis, silymarin 420 mg/day had a significantly beneficial effect on patient survival rate (compared with patients receiving placebo) in 1 randomised, double-blind trial in patients with alcoholic cirrhosis. Silymarin 420 mg/day was also shown to improve indices of liver function [AST, ALT, gamma-glutamyl transferase and bilirubin] in patients with liver disease of various aetiology, including those exposed to toxic levels of toluene or xylene; however, it was largely ineffective in patients with viral hepatitis. Reports of adverse events while receiving silymarin therapy are rare. However, there have been accounts of nausea, epigastric discomfort, arthralgia, pruritus, headache and urticaria. Silymarin has also been reported to have possibly caused a mild laxative effect. CONCLUSION: The antioxidant properties of silymarin (a mixture of at least 4 closely related flavonolignans, 60 to 70% of which is a mixture of 2 diastereomers of silybin) have been demonstrated in vitro and in animal and human studies. However, studies evaluating relevant health outcomes associated with these properties are lacking. Although silymarin has low oral absorption, oral dosages of 420 mg/day have shown some therapeutic potential, with good tolerability, in the treatment of alcoholic cirrhosis. Moreover, silybin 20 to 48 mg/kg/day has shown promise as an antidote for acute mushroom poisoning by Amanita phalloides; however, further studies paying attention to the amount of ingested mushroom and time elapsed before administration of treatment are needed to clarify its role in this indication. Studies in patients with the early onset of liver disease may demonstrate the liver regeneration properties that silymarin is promoted as possessing.

Drugs 2001;61(14):2035-63 Related Articles, Books, LinkOut


The use of silymarin in the treatment of liver diseases.

Saller R, Meier R, Brignoli R.

Abteilung Naturheilkunde, University Hospital Zurich, Switzerland.

The high prevalence of liver diseases such as chronic hepatitis and cirrhosis underscores the need for efficient and cost-effective treatments. The potential benefit of silymarin (extracted from the seeds of Silybum marianum or milk thistle) in the treatment of liver diseases remains a controversial issue. Therefore, the objective of this review is to assess the clinical efficacy and safety of silymarin by application of systematic approach. 525 references were found in the databases, of which 84 papers were retained for closer examination and 36 were deemed suitable for detailed analysis. Silymarin has metabolic and cell-regulating effects at concentrations found in clinical conditions, namely carrier-mediated regulation of cell membrane permeability, inhibition of the 5-lipoxygenase pathway, scavenging of reactive oxygen species (ROS) of the R-OH type and action on DNA-expression, for example, via suppression of nuclear factor (NF)-kappaB. Pooled data from case record studies involving 452 patients with Amanita phalloides poisoning show a highly significant difference in mortality in favour of silibinin [the main isomer contained in silymarin] (mortality 9.8% vs 18.3% with standard treatment; p < 0.01). The available trials in patients with toxic (e.g. solvents) or iatrogenic (e.g. antispychotic or tacrine) liver diseases, which are mostly outdated and underpowered, do not enable any valid conclusions to be drawn on the value of silymarin. The exception is an improved clinical tolerance of tacrine. In spite of some positive results in patients with acute viral hepatitis, no formally valid conclusion can be drawn regarding the value of silymarin in the treatment of these infections. Although there were no clinical end-points in the four trials considered in patients with alcoholic liver disease, histological findings were reported as improved in two out of two trials, improvement of prothrombin time was significant (two trials pooled) and liver transaminase levels were consistently lower in the silymarin-treated groups. Therefore, silymarin may be of use as an adjuvant in the therapy of alcoholic liver disease. Analysis was performed on five trials with a total of 602 patients with liver cirrhosis. The evidence shows that, compared with placebo, silymarin produces a nonsignificant reduction of total mortality by -4.2% [odds ratio (OR) 0.75 (0.5 - 1.1)]; but that, on the other hand, the use of silymarin leads to a significant reduction in liver-related mortality of-7% [OR: 0.54 (0.3 - 0.9); p < 0.01]. An individual trial reported a reduction in the number of patients with encephalopathy of -8.7% [p = 0.06). In one study of patients with cirrhosis-related diabetes mellitus, the insulin requirement was reduced by -25% [p < 0.01). We conclude that available evidence suggests that silymarin may play a role in the therapy of [alcoholic) liver cirrhosis. Silymarin is has a good safety record and only rare case reports of gastrointestinal disturbances and allergic skin rashes have been published. This review does not aim to replace future prospective trials aiming to provide the 'final' evidence of the efficacy of silymarin.


Effects of silymarin flavonolignans and synthetic silybin derivatives on estrogen and aryl hydrocarbon receptor activation.

Pliskova M, Vondracek J, Kren V, Gazak R, Sedmera P, Walterova D, Psotova J, Simanek V, Machala M.

Veterinary Research Institute, Brno, Czech Republic.

Silymarin, a standardized mixture of flavonolignans, or its major constituents could be effective for prevention and treatment of hepatic damage or skin cancer. However, their potential side effects, such as modulation of endocrine functions via the disruption of estrogen receptor (ER) and/or aryl hydrocarbon receptor (AhR) activation, are largely unknown. In the present study, we investigated impact of silymarin, its constituents and a series of their synthetic derivatives on ER- and AhR-mediated activities using in vitro reporter gene assays. We found that none of the compounds under study affected the AhR-mediated activity in rat hepatoma cells. Contrary to that, several compounds behaved as either partial or full ER agonists. Silymarin elicited partial ER activation, with silybin B being probably responsible for a majority of the weak ER-mediated activity of silymarin; silybin A and other flavonolignans were found to be inactive and potent ER agonist taxifolin is only a minor constituent of silymarin. To our knowledge, this is probably the first time, when receptor-specific in vitro effects of separated diastereomers have been demonstrated. In contrast to silymarin constituents, the synthetic silybin derivatives, potentially useful as chemoprotective agents, did not modulate the ER-mediated activity, with exception of 23-O-pivaloylsilybin. Interestingly, 7-O-benzylsilybin potentiated ER-mediated activity of 17beta-estradiol despite possessing no estrogenic activity. In conclusion, our data suggest that estrogenicity of some silymarin constituents should be taken in account as their potential side effect when considered as chemopreventive compounds. These results also stress the need to study biological activities of purified or synthesized diastereomers of silybin derivatives.

4cc

[Big'r]

Origineel gepost door MrJ

Nice.
Als je je post edit dat de smileys uitstaan verplaats ik hem even naar de Leerzame Threads sectie.

Ok. Heb wat dingen veranderd.

[WINSTROLST]

welke dosering dien je die mariadistel dan te nemen ?

[endymion]

Origineel gepost door WINSTROLST

welke dosering dien je die mariadistel dan te nemen ?

Op het potje staat 3 capsules per dag (250 mg)

[Big'r]

Origineel gepost door WINSTROLST

welke dosering dien je die mariadistel dan te nemen ?

Afhankelijk van de hoeveelheid roids tijdens de kuur zou ik zelf voor 2-3 weken 500 mg/dag gaan.

Wanneer je geel uitslaat (wat af en toe wil gebeuren bij overgevoelige mensen of onverantwoord gebruik), zou ik er zelf gedurende een aantal weken 1000 mg in rammen!

[Big T]

Idd goed product, en niet chemisch wat een grote plus is.

Wel na de kuur niet tijdens idd.

[enrico01]

wat moet je maria destel niet tijdens een kuur nemen ik gebruik nu deca en d-anabool,maria distel helpt toch je lever te reinigen??of zie ik dat verkeerd trouwens mijn kuur gaat supper 3de week nog 7 te gaan en ik krijg nu al van mensen te hoen dat ik ben gegroeit,en ze weten niks over het kuren zelf merk ik het ook maar het is niet echt dat je zecht wooow maar dat komt omdat ik 10 keer per dag ik de spiegel kijk heheheh graag meer uit leg over maria distel in het nederlands aub alvast bedankt mensen

[Br0]

Als je mariadistel nu al tijdens de kuur gaat gebruiken, terwijl je aan de tabs zit. Dan gaat je lever de stoffen nog meer gaan afbreken waardoor je minder werkzaamstof in je hebt. Daarom dat je mariadistel alleen maar na je NAkuur mag gebruiken. (en niet vlak na de kuur, want je moet ook nog nakuren met nolva/clomid wat ook in tabvorm is).

[ECLIPSE]

geldt dit alleen voor tabs? ^o)

[Ruff-E]

Origineel gepost door ECLIPSE

geldt dit alleen voor tabs? ^o)

Yep, de invloed van silymarin op injectables in te verwaarlozen. Daarom kun je best tijdens je cycle mariadistel slikken zolang je er maar voor zorgt dat je begint ná de oral en eindigt vóór de PCT.

[ECLIPSE]

oh dat is interressant, kun je dit verder beargumenteren/ondersteunen?