Let's be honest, does Milk Thistle even do anything?

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    Let's be honest, does Milk Thistle even do anything?


    It looks like to me that there's more than a handful of guys who'll take pro-hormones or roids and they'll take milk thistle and think that everything will be alright.

    From what I can tell off of google searches on quite a few sites is that there seems to be a lack of scientific evidence and the mayo clinic's site goes along with this.

    I'd be happy if someone can refute this for me.

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    Quote Originally Posted by Matt Skiba View Post
    It looks like to me that there's more than a handful of guys who'll take pro-hormones or roids and they'll take milk thistle and think that everything will be alright.

    From what I can tell off of google searches on quite a few sites is that there seems to be a lack of scientific evidence and the mayo clinic's site goes along with this.

    I'd be happy if someone can refute this for me.
    The only studies I've seen that show any benefit indicate that if it should be used for a long time (post damage) then it may help the liver in the repair process. In no way does it protect the liver from damage. From those studies it seems that if it is started it should be continued for a month or more post cycle and then it may provide a benefit. I saw a study once that indicated that it could do more harm then good it it were discontinued during the repair process.

    But yes I agree w/ you. Most oral steroids and pro-hormones cause liver damage no matter what...the damage can not be lessened or eliminated...it must be repaired and it looks like it is up to the liver to repair itself.
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    Quote Originally Posted by Matt Skiba View Post
    It looks like to me that there's more than a handful of guys who'll take pro-hormones or roids and they'll take milk thistle and think that everything will be alright.

    From what I can tell off of google searches on quite a few sites is that there seems to be a lack of scientific evidence and the mayo clinic's site goes along with this.

    I'd be happy if someone can refute this for me.
    Milk Thistle's main active bioconstituent is Silymarin. Silymarin selectively acts as an anti-oxidant and protects the bile duct from free radical damage specifically in the intestines and stomach. It increases the liver's content of GSH (glutathione) which is a substance in detoxifying many potentially damaging hormones, chemicals, and drugs (including acetaminophen) It has demonstrated a membrane stabilizing action, which inhibits or prevents lipid peroxidation. It seems to alter the structures of outer wall membranes of hepatocytes, preventing penetration of liver poisons and stimulates the action of nuclear polymerase A. It may increase ribosomal protein synthesis and stimulate the formation of new hepatocytes.
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    Matt-


    You might catch flak on this one. I've always have been skeptical about Milk Thistle, and I'm not going to say it does not do anything, but honestly you think your liver was equally as fine after taking M1T just because you used Milk Thistle ?

    I really doubt its effectiveness and you'll get a bunch of people going here's some studies, blah, blah, blah but in my personal opinion I think it is useless against harsh hepatoxic steroids. You're better off just using injectables.
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    Molecular Epidemiology and Cancer Prevention


    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
    Jifu Zhao1 and Rajesh Agarwal1,2,3

    1 Center for Cancer Causation and Prevention, AMC Cancer Research Center, Denver, CO 80214 and
    2 University of Colorado Cancer Center, University of Colorado Health Sciences Center, Denver, CO 80262, USA


    Abstract
    Top
    Abstract
    Introduction
    Materials and methods
    Results
    Discussion
    References


    Polyphenolic antioxidants are being identified as cancer preventive agents. Recent studies in our laboratory have identified and defined the cancer preventive and anticarcinogenic potential of a polyphenolic flavonoid antioxidant, silymarin (isolated from milk thistle). More recent studies by us found that these effects of silymarin are due to the major active constituent, silibinin, present therein. Here, studies are done in mice to determine the distribution and conjugate formation of systemically administered silibinin in liver, lung, stomach, skin, prostate and pancreas. Additional studies were then performed to assess the effect of orally administered silibinin on phase II enzyme activity in liver, lung, stomach, skin and small bowel. For tissue distribution studies, 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. The desired tissues were collected, homogenized and parts of the homogenates were extracted with butanol:methanol followed by HPLC analysis. The column eluates were detected by UV followed by electrochemical detection. The remaining homogenates were digested with sulfatase and -glucuronidase followed by analysis and quantification. Peak levels of free silibinin were observed at 0.5 h after administration in liver, lung, stomach and pancreas, accounting for 8.8 1.6, 4.3 0.8, 123 21 and 5.8 1.1 (mean SD) g silibinin/g tissue, respectively. In the case of skin and prostate, the peak levels of silibinin were 1.4 0.5 and 2.5 0.4, respectively, and were achieved 1 h after administration. With regard to sulfate and -glucuronidate conjugates of silibinin, other than lung and stomach showing peak levels at 0.5 h, all other tissues showed peak levels at 1 h after silibinin administration. The levels of both free and conjugated silibinin declined after 0.5 or 1 h in an exponential fashion with an elimination half-life (t) of 57–127 min for free and 45–94 min for conjugated silibinin in different tissues. In the studies examining the effect of silibinin on phase II enzymes, oral feeding of silibinin at doses of 100 and 200 mg/kg/day showed a moderate to highly significant (P < 0.1–0.001, Student's t-test) increase in both glutathione S-transferase and quinone reductase activities in liver, lung, stomach, skin and small bowel in a dose- and time-dependent manner. 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, and suggest further studies to assess the cancer preventive and anticarcinogenic effects of silibinin in different cancer models.


    Abbreviations: CDNB, 1-chloro-2,4-dinitrobenzene; DCP-IP, 2,6-dichlorophenol-indophenol; EC, electrochemical; GST, glutathione S-transferase; OSA, 1-octanesulfonic acid; QR, quinone reductase; TEA, triethylamine; TPA, 12-O-tetradecanoylphorbol-13-acetate.


    Introduction
    Top
    Abstract
    Introduction
    Materials and methods
    Results
    Discussion
    References


    Silymarin, a polyphenolic flavonoid isolated from the seeds of milk thistle [Silybum marianum (L.) Gaertn] (1), is composed mainly of silibinin (or silybin, Figure 1) with small amounts of other silibinin stereoisomers, namely isosilybin, dihydrosilybin, silydianin and silychristin (2). Silymarin and silibinin are used clinically in Europe and Asia for the treatment of liver diseases (ref. 3 and references therein). In patients with liver disorders, treatment with silymarin or silibinin has been shown to improve liver function more rapidly than in those receiving placebo (4). Another multicenter trial showed that 420 mg daily administration of silymarin for several years resulted in a significant reduction in the mortality of patients suffering from alcoholic liver cirrhosis (5). The human population in Europe have used silymarin or silibinin as a liver tonic and current research indicates that it can be used in a whole range of liver and gall bladder conditions, including hepatitis and cirrhosis as well as dermatological conditions (6,7). In more recent years, silymarin has been marketed in the USA and Europe as a dietary supplement.





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    Oxford Journals Contact Us My Basket My Account CarcinogenesisAbout This Journal Contact This Journal Subscriptions Current Issue Archive Search Oxford Journals Life Sciences Carcinogenesis Volume 20, Number 11 Pp. 2101-2108
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    Carcinogenesis, Vol. 20, No. 11, 2101-2108, November 1999
    1999 Oxford University Press

    --------------------------------------------------------------------------------

    Molecular Epidemiology and Cancer Prevention


    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
    Jifu Zhao1 and Rajesh Agarwal1,2,3

    1 Center for Cancer Causation and Prevention, AMC Cancer Research Center, Denver, CO 80214 and
    2 University of Colorado Cancer Center, University of Colorado Health Sciences Center, Denver, CO 80262, USA


    Abstract
    Top
    Abstract
    Introduction
    Materials and methods
    Results
    Discussion
    References


    Polyphenolic antioxidants are being identified as cancer preventive agents. Recent studies in our laboratory have identified and defined the cancer preventive and anticarcinogenic potential of a polyphenolic flavonoid antioxidant, silymarin (isolated from milk thistle). More recent studies by us found that these effects of silymarin are due to the major active constituent, silibinin, present therein. Here, studies are done in mice to determine the distribution and conjugate formation of systemically administered silibinin in liver, lung, stomach, skin, prostate and pancreas. Additional studies were then performed to assess the effect of orally administered silibinin on phase II enzyme activity in liver, lung, stomach, skin and small bowel. For tissue distribution studies, 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. The desired tissues were collected, homogenized and parts of the homogenates were extracted with butanol:methanol followed by HPLC analysis. The column eluates were detected by UV followed by electrochemical detection. The remaining homogenates were digested with sulfatase and -glucuronidase followed by analysis and quantification. Peak levels of free silibinin were observed at 0.5 h after administration in liver, lung, stomach and pancreas, accounting for 8.8 1.6, 4.3 0.8, 123 21 and 5.8 1.1 (mean SD) g silibinin/g tissue, respectively. In the case of skin and prostate, the peak levels of silibinin were 1.4 0.5 and 2.5 0.4, respectively, and were achieved 1 h after administration. With regard to sulfate and -glucuronidate conjugates of silibinin, other than lung and stomach showing peak levels at 0.5 h, all other tissues showed peak levels at 1 h after silibinin administration. The levels of both free and conjugated silibinin declined after 0.5 or 1 h in an exponential fashion with an elimination half-life (t) of 57–127 min for free and 45–94 min for conjugated silibinin in different tissues. In the studies examining the effect of silibinin on phase II enzymes, oral feeding of silibinin at doses of 100 and 200 mg/kg/day showed a moderate to highly significant (P < 0.1–0.001, Student's t-test) increase in both glutathione S-transferase and quinone reductase activities in liver, lung, stomach, skin and small bowel in a dose- and time-dependent manner. 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, and suggest further studies to assess the cancer preventive and anticarcinogenic effects of silibinin in different cancer models.


    Abbreviations: CDNB, 1-chloro-2,4-dinitrobenzene; DCP-IP, 2,6-dichlorophenol-indophenol; EC, electrochemical; GST, glutathione S-transferase; OSA, 1-octanesulfonic acid; QR, quinone reductase; TEA, triethylamine; TPA, 12-O-tetradecanoylphorbol-13-acetate.


    Introduction
    Top
    Abstract
    Introduction
    Materials and methods
    Results
    Discussion
    References


    Silymarin, a polyphenolic flavonoid isolated from the seeds of milk thistle [Silybum marianum (L.) Gaertn] (1), is composed mainly of silibinin (or silybin, Figure 1) with small amounts of other silibinin stereoisomers, namely isosilybin, dihydrosilybin, silydianin and silychristin (2). Silymarin and silibinin are used clinically in Europe and Asia for the treatment of liver diseases (ref. 3 and references therein). In patients with liver disorders, treatment with silymarin or silibinin has been shown to improve liver function more rapidly than in those receiving placebo (4). Another multicenter trial showed that 420 mg daily administration of silymarin for several years resulted in a significant reduction in the mortality of patients suffering from alcoholic liver cirrhosis (5). The human population in Europe have used silymarin or silibinin as a liver tonic and current research indicates that it can be used in a whole range of liver and gall bladder conditions, including hepatitis and cirrhosis as well as dermatological conditions (6,7). In more recent years, silymarin has been marketed in the USA and Europe as a dietary supplement.





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    Fig. 1. Chemical structure of silibinin.




    In vivo pretreatment of experimental animals with silymarin or silibinin has been shown to protect against hepatotoxicity induced by a wide range of toxicants, including allylalcohol, carbon tetrachloride, galactosamine, phalloidin, thioacetamide and microcystin-LR (refs 138 and references therein). Other in vivo studies employing animal models and in vitro studies utilizing hepatocytes and liver microsomes have shown that both silymarin and silibinin afford significant protection against liver reduced glutathione depletion and lipid peroxidation induced by xenobiotic agents (9–12). Mechanistic studies in rodents and in cell culture have shown that silymarin is a strong antioxidant capable of scavenging free radicals (13–17). Besides, limited in vitro studies have shown that silymarin inhibits: (i) the formation of transformed rat tracheal epithelial cell colonies induced by exposure to benzo[a]pyrene (18); (ii) 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced anchorage-independent growth of JB6 mouse epidermal cells (19); (iii) 7,12-dimethylbenz[a]anthracene-initiated and TPA-promoted mammary lesion formation in organ culture (20).
    Based on the strong antioxidant activity of silymarin and the fact that silymarin and silibinin are already being used clinically as therapeutic agents, we started studies assessing the cancer chemopreventive and anticarcinogenic effects of silymarin in both long-term animal protocols and short-term cell culture models. Studies published in recent years from our laboratory showed that: (i) silymarin inhibits skin tumor promoter induction of ornithine decarboxylase activity and mRNA expression in mouse epidermis (21); (ii) topical application of silymarin protects significantly against UVB radiation-induced non-melanoma skin cancers in mice and that this effect of silymarin largely involves inhibition of UVB radiation-induced ornithine decarboxylase and cyclooxygenase activities, sunburn cell formation and skin edema (22); (iii) topical application of silymarin results in a highly significant to complete protection against skin tumor promoter-caused papilloma formation in mouse skin (23,24); (iv) silymarin inhibits the growth and proliferation of human cervical, breast and prostate carcinoma cells by inhibiting mitogenic signaling and inducing perturbations in cell cycle progression (25–27). More recently, studies from our laboratory have shown that silibinin, the major active constituent present in silymarin, has comparable (to silymarin) inhibitory effects towards human prostate, breast and cervical carcinoma cell growth, DNA synthesis and cell viability and is as strong an antioxidant as silymarin (N.Bhatia, J.Zhao and R.Agarwal, manuscript under review). Taken together, these studies suggested that both silymarin and silibinin have the potential to be developed as preventive and interventive agents against several human cancers. Despite a wide range of studies with both silymarin and silibinin and their clinical usage, the biodistribution and metabolism of silymarin and silibinin have not been studied in experimental animals. As a part of our systematic cancer chemopreventive and anticarcinogenic studies with silymarin and silibinin, in the present study we have assessed the tissue distribution and conjugate formation of systemically administered silibinin in mice. Additional studies were also performed to assess the effect of orally administered silibinin on the levels of phase II enzymes in different mouse tissues.


    Materials and methods
    Top
    Abstract
    Introduction
    Materials and methods
    Results
    Discussion
    References


    Animal treatment with silibinin for tissue distribution studies
    Six to seven-week-old male SENCAR mice were purchased from the National Cancer Institute (Frederick Cancer Research and Development Center, Frederick, MD). The animals were housed five per cage at 24 2C and 50 10% relative humidity and subjected to a 12 h light/12 h dark cycle. They were acclimatized for 1 week before use in the present study and fed a Purina chow diet and water ad libitum. Prior to the study, the dorsal side of the skin was shaved using electric clippers to facilitate skin homogenization for silibinin extraction. The animals were starved for 24 h prior to dosing and were hydrated with 0.5 ml of tap water by intragastric intubation 1 h before administration of silibinin. Each time point had five mice. Silibinin, obtained commercially from Sigma Chemical Co. (St Louis, MO), was dissolved as 1.5 mg/ml silibinin in a water-based dosing solution containing 0.9% sodium chloride (w/v), 3% ethanol (v/v), 1% Tween 80 (v/v) and 6.6 mM sodium hydroxide. To make this solution, silibinin was first completely dissolved in the desired volume of ethanol and Tween 80 and then diluted with sodium chloride and sodium hydroxide solutions to achieve the final dosing solution detailed above. Silibinin (at a dose of 50 mg/kg body wt) was administered orally by feeding needle. A group of five mice was also similarly administered vehicle only and served as a negative control for tissue recovery studies. At different times after silibinin administration, mice were killed and liver, lung, stomach, skin, prostate and pancreas were removed. Each tissue sample was quickly snap frozen in liquid nitrogen and stored at –80C until further analysis. Control mice were killed 1 h after the vehicle treatment and the desired tissues were removed and stored at –80C.

    Extraction of free and conjugated silibinin from different tissues
    Each tissue sample obtained from different silibinin treatment time points was assessed for both free and conjugated forms of silibinin. Briefly, tissues (50–150 mg) were suspended in 3 vol of 50 mM Tris–HCl, pH 7.4, and homogenized thoroughly at room temperature using a Polytron PT-10 homogenizer (VWR Scientific, Plainfield, NJ). Each homogenate was divided into two parts. One part (80% of the total homogenate) was added to an equal volume of butanol:methanol (95:5 v/v) and mixed with the homogenizer for 5 s. The samples were centrifuged at 1500 r.p.m. at 4C for 5 min and the organic layer collected. The butanol:methanol extraction was repeated twice more and the three butanol extracts were combined and stored at –80C until HPLC analysis. The remaining tissue homogenate (20% of the total homogenate) was added to 100 l of enzyme solution containing 500 U of -glucuronidase and 40 U of sulfatase (both from Sigma Chemical Co.) in 50 mM Tris–HCl, pH 7.4. The solution was incubated at 37C for 1.5 h and then extracted with the same volume of butanol:methanol (95:5 v/v) three times. The three butanol extracts were combined and stored at –80C until HPLC analysis.

    HPLC analysis
    The HPLC system (ESA, Bedford, MA) consisted of two ESA 580 model pumps, a UV detector, an electrochemical (EC) detector and ESA 5600 model HPLC control and analysis software. The UV detection wavelength was set at 270 nm and the potential for EC detection was 500 mV. An ESA C18 reversed phase analytical column (3 m, 4.6x250 mm) was employed in all the HPLC analyses. The HPLC mobile phase contained solvent A [7.5% methanol in 100 mM acetate buffer containing 50 mM triethylamine (TEA) and 1 mM 1-octanesulfonic acid (OSA), pH 4.8] and solvent B (80% methanol in 100 mM acetate buffer containing 50 mM TEA and 1 mM OSA, pH 4.8). The linear gradient system employed at room temperature was: 0–5 min, 75% solvent A and 25% solvent B; 5–15 min, 75% solvent A and 25% solvent B to 50% of both solvents A and B; 15–20 min, 50% of solvents A and B to 30% solvent A and 70% solvent B; 20–25 min, isocratic 30% solvent A and 70% solvent B; 25 min, end of run. The solvent flow rate throughout the HPLC run was 0.6 ml/min and the column eluate was monitored by UV absorbance at 270 nm followed by EC detection.

    Before the analysis and quantification of free and conjugated silibinin extracted from tissue samples, different concentrations of standard silibinin were analyzed by HPLC to find the quantitative linear range for both UV and EC detection. As needed, every tissue sample extract was adjusted to make sure that the amount of silibinin was within the linear range of detection. In each case, a 20 l tissue extract was initially injected into the HPLC column and the silibinin peak was detected by the UV detector (270 nm) and further confirmed by the EC detector (500 mV). Silibinin quantification was based on peak area under the curve analysis and comparison with standard silibinin. The recovery of silibinin following extraction from different tissue homogenates was checked by adding a known amount of silibinin to each tissue homogenate and, following vigorous mixing, its extraction and quantification by HPLC as detailed above. In order to quantify the levels of conjugated silibinin in different tissue samples, the total silibinin levels obtained from enzyme-digested tissue homogenates were corrected for the levels of free silibinin. In all cases, therefore, the data shown for conjugated silibinin are after subtraction of free silibinin concentrations.

    Animal treatment with silibinin for phase II enzyme studies
    Six to seven-week-old female SENCAR mice were used in the study and housed in the animal facility as detailed above. The animals were acclimatized for 1 week before use in the present study and fed a Purina chow diet and water ad libitum. Several different studies in the past have used different doses, modes of administration and solutions/suspensions of silymarin or silibinin in rodent studies (refs 1, 3, 8–11 and references therein). These include doses from as low as 8 mg/kg/day for 10 days to as high as 1500 mg/kg once; administered i.p., intragastrically, p.o., i.v., etc., and dissolved in Tween 80/water, suspended in water, suspended in carboxymethyl cellulose, dissolved in saline or 0.1 N sodium hydroxide, etc. (1,3,8–11). Based on all these studies, for the phase II enzyme studies reported here we selected two doses of silibinin, 100 and 200 mg/kg body wt, and administered them by oral intubation dissolved in 0.2 ml of cottonseed oil. The animals in control groups were administered an equal amount of cottonseed oil only by oral intubation. Each time point and treatment group had five mice. The animal treatments with the above-mentioned doses of silibinin or cottonseed oil alone were done once in the morning every day and 24 h after 3, 7 and 15 days mice in each group were killed and liver, lung, stomach, skin and small bowel were removed and immediately placed in ice-cold 0.1 M phosphate buffer, pH 7.4. Tissues were cleaned properly, minced and homogenized in the same buffer and 100 000 g supernatant fractions were prepared as described earlier (28). Glutathione S-transferase (GST) activity was determined according to Habig et al. (29) using 1-chloro-2,4-dinitrobenzene (CDNB) as substrate. Quinone reductase (QR) activity was determined as described by Benson et al. (30) using 2,6-dichlorophenol-indophenol (DCP-IP) as electron acceptor. The statistical significance of differences in enzyme activities between cottonseed oil-treated controls and two doses of silibinin-treated experimental groups was analyzed using Student's t-test. Throughout the feeding protocol of silibinin in cottonseed oil or vehicle alone, animals were watched for any apparent signs of toxicity and food and water consumption. No evident change was observed in these mice throughout the experimental protocols (results not shown).


    Results
    Top
    Abstract
    Introduction
    Materials and methods
    Results
    Discussion
    References


    HPLC standardization and linear range of silibinin detection
    First we standardized the HPLC conditions and both UV and EC detection sensitivity in the linear range. For these, different amounts of commercially obtained silibinin were dissolved in HPLC grade n-butanol and subjected to HPLC separation under different solvent gradient conditions. As shown in Figure 2A, under the HPLC method and solvent gradient system detailed in Materials and methods we were able to detect commercially obtained silibinin as a single peak by both 270 nm UV absorbance and by EC detection. In both cases, silibinin characteristically showed a retention time of ~13.5 min (Figure 2A). These HPLC profiles of silibinin also show its purity as 100%. Based on these HPLC profiles of silibinin, a linear detection range of silibinin under these conditions was also sought. As shown in Figure 2B, the standard curve for silibinin was linear in the range 10–100 ng in the case of UV detection (r = 0.9999) and 4–120 ng in the case of EC detection (r = 0.9999). Whereas the sensitivity of EC detection was much higher than that of UV detection, EC detection showed a high level of variation in detection limits, possibly because of a small change in room temperature or a change of solvent (data not shown), although OSA and TEA were used in the solvents to improve EC detection sensitivity and stability. Because of this, those tissue extract samples which were found to have a high concentration of silibinin were quantified using UV detection, whereas for samples with a low concentration of silibinin EC quantification was used
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    http://carcin.oxfordjournals.org/cgi...ull/20/11/2101

    Ok all the graphs are not showing up when I paste this so here is the article link.
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    Ok I see the studies. Here's my question to everyone who is pro-milk thistle.

    1. Do you know specifically how the 17a methylation of a oral affects the liver ?

    2. Comparing acetominophen to anadrol/dianabol are not the same thing. A painkiller that is not methylated is different from a methylated oral. While both create problematic effects upon the liver their mechanism is different. If you can find a study indicating the difference between the 2 then I'll be willing to reconsider.
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    BTW, for articles about milk thistle, please keep them to ONLY the ones regarding Milk Thistle+orals.

    In my opinion everything else is irrelevant because we are talking about different compounds.

    acetominophen to dianabol is comparing apples to oranges. It just does not work.
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    Quote Originally Posted by ReaperX View Post
    BTW, for articles about milk thistle, please keep them to ONLY the ones regarding Milk Thistle+orals.

    In my opinion everything else is irrelevant because we are talking about different compounds.

    acetominophen to dianabol is comparing apples to oranges. It just does not work.
    Actually they do work. He wanted to know whether Milk Thistle actually did anything for the liver.
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    truth be told, it's more preventative and has to be used over a long period of time.

    as this has been covered over and over again, milk thistle will not "save" your liver from something as harsh as M1T, but in conjunction with BCAAs and NAC, Silymarin will help curb some of the damage.
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    I've been using milk thistle pretty much continuously since 1990, and I feel like it does work but like vitamins and other antioxidents, they must be used for long perios of time to mitigate the damage. Nothing will magically shield the liver, but its regenerative powers are amazing considering the things we put in our bodies and ask it to deal with.
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    Milk thistle seemed to clear my skin up for a bit, and then it made me break out worse than ever, before I even stopped taking it.
  

  
 

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