Silymarin - has anyone taken this ?

I have a good friend with a young wife at 33 who has Stage IV in-operaple liver cancer. She is currently undergoing Chemo (Tac) Xeloda and other weekly infusion of which I am unsure. She was born with Hep B.

My question is here has anyone used Silymarin as a supplement to improve efficacy and prognosis for liver cancer and or precancerous conditions ?

If not, I am curious why people have not been made aware of this naturally occurring substance that has been used for 2000+ years.

There is ample information available but I found one interesting study (See link) showing very positive results. While it doesn't do everything, it does a hell of lot of good things for liver conditions.

http://cancerres.aacrjournals.org/content/68/6/2033.full

http://en.wikipedia.org/wiki/Silibinin

I Look FWD to hearing any feedback.

Scambuster
(Crossover from the H&N board)

Extract on Silymarin

http://www.hepatitis-central.com/hcv/herbs/products/challenge.htmlSilymarin. A standardized extract from the milk thistle Silybum marianum contains as its main constituents the flavonoids silybinin, silydianin, and silychristin.24 Milk thistle extracts were used as early as the 4th century B.C., became a favored medicine for hepatobiliary diseases in the 16th century, and experienced a revival in central Europe in the late 1960s (table 2). The flavonoid silibinin, which constitutes 60% to 70% of silymarin, has been identified as the major active ingredient.25,26 Its pharmacological profile is well defined, and studies in cell culture and animal models clearly show its hepatoprotective action with little or no toxicity.26,27,33-41 Silymarin enhances the activity of hepatocyte RNA-polymerase I,26 complexes toxic free iron,33 protects the cell membrane from radical-induced damage,34 and blocks the uptake of toxins such as Amanita phalloides toxin.32,35 A potent scavenger, it prevents lipid peroxidation and normalizes the lipid profile of hepatocyte membranes.36 Silymarin provided liver protection in rat models of liver damage induced by carbon tetrachloride and paracetamol.37,38 Four of 12 dogs fed lyophilized Amanita toxin and given supportive care died from hepatic failure and coma within 35 to 54 hours, whereas all 11 dogs receiving high-dose silymarin survived.39 In a retrospective analysis of 205 patients with Amanita intoxication, of whom 30 received treatment, the death rate of those given intravenous silymarin was reduced significantly (12.8% vs. 22.4%).40

To View This table

table 2. History of the Milk Thistle as a Liver Remedy
In recent in vitro studies, silymarin down-regulated the proinflammatory leukotriene B4 in Kupffer cells.41 In randomized clinical trials for acute viral hepatitis A or B, oral silymarin either exerted no benefit29 or accelerated clinical recovery, causing a significantly more rapid normalization of bilirubin and aspartate transaminase than did the control.30 Similarly, in alcohol-related hepatitis treated with silymarin, transaminase levels dropped more rapidly than in the untreated disease.42 A 4-month course of silymarin in patients with moderately active alcohol-related liver disease led to a 41% reduction of alanine transaminase, compared with no change in controls.43 In a randomized trial, 170 biopsy-proven cirrhotic patients, 92 with alcohol-related and 78 with nonalcohol-related liver disease, were treated with silymarin or placebo for a mean of 41 months.44 Although serum biochemistry values did not differ between the 2 groups, the number of surviving cirrhotic patients with alcohol-related liver disease was significantly higher in the silymarin group, especially in those with Child-Pugh class A cirrhosis. Most of the latter patients continued to drink, which may have influenced the results. Also, the dropout rate was high, although dropouts were counted as therapy failures. A subsequent randomized, placebo-controlled study of 200 patients with alcohol-related cirrhosis, 75 of whom dropped out, could not confirm a survival benefit.45

These data point up the difficulty of studying a heterogeneous group of patients and of using death as the endpoint for a condition that progresses over many years. An intermediate endpoint is progression of fibrosis to cirrhosis, which is the primary determinant of morbidity and mortality in patients with chronic liver diseases. In vitro, silymarin blocks proliferation of hepatic stellate cells, the main source of excess collagen in fibrosis. This is accompanied by down-regulation of the profibrogenic transforming growth factor .46 In liver injury induced by complete occlusion of the biliary system in the rat, oral silymarin reduced collagen accumulation in a dose-dependent fashion.47 It was similarly antifibrotic when administered from weeks 4 to 6, i.e., starting at a time when liver collagen is already increased 4-fold, a situation encountered in most patients with chronic liver disease. The antifibrotic effect was accompanied by reduced numbers of activated stellate cells48 and a greater than 50% reduction of both procollagen I and tissue inhibitor of metalloproteinase messenger RNA, both being major effectors of fibrogenesis.49 These data have spawned randomized, placebo-controlled studies of silymarin in patients with chronic viral hepatitis that include follow-up biopsies and a panel of serum markers of liver fibrosis.50