Liver Pills do not protect the liver!
05-25-2006 12:15 AM
Liver Pills do not protect the liver!
The liver protectant pills that are advertised to protect our livers while on AAS or PH's are the epitome of a snake oil sale.
People keep suggesting on this board, and other forums, that liver pills be taken to ensure safety during a cycle. I am NOT an expert on steroids, how they work or any of the stuff like that, but I a premed student and I talked to my dad, who has been a psychiatrist for over 30 years.
The doc looked at my liver protectant bottle and explained to me that there is nothing available today that can actually coat the liver from harsh toxins.
I asked my dad if it was possible that doctors would say this because they are against the use of steroids without a prescription, and try to discourage use anyway possible. To this he responded.
"The medical community would have a bias to anything that would protect the liver. We prescribe medications everyday that are extremly heptatoxic. I think if something were available that actually worked, that a medical journal would write about it."
My dad went on to explain the theory of these so called liver protectants, and how they could not work. He than pointed to my bottle and read off this line from it: "These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or PREVENT ANY DISEASE."
"Which is it," my dad replied. "They say this protects the liver, but than say here that it does not prevent any disease."
My dad went on to say that best case scenario these pills will do nothing. He was not convinced of this however.
"It is possible that these pills do affect the liver. However there has never been a study of them of any size. It is possible that these pills do affect the liver, but in a negative way. No one knows, because they are not studied."
05-25-2006 12:23 AM
Originally Posted by Umpire10589
05-25-2006 12:28 AM
Originally Posted by Umpire10589
Sigh, as a pre-med student, you're probably learning something about the scientific method. Sadly, what you've done here is commit a basic logic flaw. You've asserted the "appeal to authority" error. Instead of saying "my dad says they're worthless and that no study has been done upon them," you might have taken a few minutes out of your life to see IF any studies had been done upon them. Doing a quick pubmed search using just ONE search term (milk thistle) turned up 185 articles from medical journals.
1: Curr Med Chem. 2006;13(9):1055-74. Related Articles, Links
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Silymarin as a new hepatoprotective agent in experimental cholestasis: new possibilities for an ancient medication.
Crocenzi FA, Roma MG.
Instituto de Fisiologia Experimental (IFISE), Facultad de Ciencias Bioquimicas y Farmaceuticas (CONICET--U.N.R.), S2002LRL, Rosario, Argentina.
Silymarin is a purified extract from milk thistle (Silybum marianun (L.) Gaertn), composed of a mixture of four isomeric flavonolignans: silibinin (its main, active component), isosilibinin, silydianin and silychristin. This extract has been empirically used as a remedy for almost 2000 years, and remains being used as a medicine for many types of acute and chronic liver diseases. Despite its routinely clinical use as hepatoprotectant, the mechanisms underlying its beneficial effects remain largely unknown. This review addresses in detail a number of recent studies showing a novel feature of silymarin as a hepatoprotective drug, namely: its anticholestatic properties in experimental models of hepatocellular cholestasis with clinical correlate. For this purpose, this review will cover the following aspects: 1. The chemistry of silymarin, including chemical composition and properties. 2. The current clinical applications of silymarin as a hepatoprotective agent, including the mechanisms by which silymarin is thought to exert its hepatoprotective properties, when known. 3. The physiological events involved in bile formation, and the mechanisms of hepatocellular cholestasis, focusing on cellular targets and mechanisms of action of drugs used to reproduce experimentally cholestatic diseases of clinical interest, in particular estrogens and monohydroxylated bile salts, where anticholestatic properties of silymarin have been tested so far. 4. The recent findings describing the impact of silymarin on normal bile secretion and its novel, anticholestatic properties in experimental models of cholestasis, with particular emphasis on the cellular/molecular mechanisms involved, including modulation of bile salt synthesis, biotransformation/depuration of cholestatic compounds, changes in transporter expression/activity, and evocation of signaling pathways.
PMID: 16611084 [PubMed - in process]
1: Dig Dis. 2005;23(3-4):275-84. Related Articles, Links
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Treatment of alcoholic liver disease.
Bergheim I, McClain CJ, Arteel GE.
Department of Pharmacology and Toxicology, University of Louisville Health Sciences Center, Louisville, KY 40292, USA.
Alcoholic liver disease (ALD) remains a major cause of morbidity and mortality worldwide. For example, the Veterans Administration Cooperative Studies reported that patients with cirrhosis and superimposed alcoholic hepatitis had a 4-year mortality of >60% (worse than many common cancers such as breast and prostate). The cornerstone for therapy for ALD is lifestyle modification, including drinking cessation and treatment of decompensation, if appropriate. Nutrition intervention has been shown to play a positive role on both an in-patient and out-patient basis. Corticosteroids are effective in selected patients with alcoholic hepatitis, and treatment with pentoxifylline appears to be a promising anti-inflammatory therapy. Recent studies have indicated anti-TNFalpha therapy, at least for alcoholic hepatitis. Some complementary and alternative medicinal agents, such as milk thistle and S-adenosylmethionine, may be effective in alcoholic cirrhosis. Treatment of the complications of ALD can improve the quality of life and, in some cases, decrease short-term mortality. Copyright 2005 S. Karger AG, Basel.
PMID: 16508292 [PubMed - in process]
1: Phytother Res. 2006 Feb;20(2):115-9. Related Articles, Links
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An in vitro study of the protective effect of the flavonoid silydianin against reactive oxygen species.
Zielinska-Przyjemska M, Wiktorowicz K.
Department of Pharmaceutical Biochemistry, Poznan University of Medical Sciences, Grunwaldzka 6, 60-780 Poznan, Poland. firstname.lastname@example.org
The inhibitory effect of silydianin, an active constituent of Silybium marianum, on the in vitro production and release of oxidative products has been examined. Polymorphonuclear neutrophils (PMNs) play a primary role in the initiation and propagation of inflammatory responses. Their apoptosis is a major mechanism associated with the resolution of inflammatory reactions. Neutrophils were assessed for caspase-3 activity, the rst step in the execution phase of apoptosis. When cells were cultured with 100 microM silydianin for 24 h, caspase-3 was activated. Induction of apoptosis by silydianin was accompanied by a decrease in luminol-enhanced chemiluminescence as well as superoxide radical (O2*-) release in freshly isolated cells and lipid peroxidation in mouse spleen microsomes. No significant effect of silydianin on PMN hydrogen peroxide production evaluated by a flow cytometric dichlorofluorescin oxidation assay was found. Such results indicate a possible antiinflammatory activity for silydianin, which regulates caspase-3 activation, affects cell membranes and acts as a free radical scavenger. Copyright 2006 John Wiley & Sons, Ltd.
PMID: 16444663 [PubMed - indexed for MEDLINE]
05-25-2006 12:29 AM
With regards to that quote I forgot to mention, that wasnt a direct argument it was merely his question of, "well which is it... do they protect you frim disease (liver inflammation), or dont they? He was merely suggesting a hypocritical message being portrayed on the bottle.
05-25-2006 12:30 AM
Hepatoprotective effects of silymarin in androgenic-anabolic steroid-induced liver damage
Med Pregl. 2003; 56 Suppl 1:79-83 (ISSN: 0025-8105)
Radovanovi? D; Jovanovi? D; Mihailovi? D; Rankovi? G; Stojiljkovi? N; Dimitrov
INTRODUCTION: The use and abuse of anabolic-androgenic steroids (AAS) commonly induces liver damage. MATERIAL AND METHODS: The study included 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. This group was not exercised nor treated, and animals received a standard amount of food for laboratory animals of this kind and age. Quantitative analysis of obtained hemataxylin-eosin, periodic acid shift and enzymohistochemical preparations was processed using Digital Image Analysis System: Microimage 3.0. RESULTS: It was established that processes in the nuclei of animals in groups M and K were significantly more intensive (p<0.001) in relation to groups M+S and C. The investigation of glycogen showed significantly higher density in the cells of groups M and M+S in comparison to groups K and C. Also, there was a significant difference between groups M+S and M. Density of enzyme activity of glutamate dehydrogenase in hepatocytes of animals in the group M+S was significantly higher in relation to the remaining three groups. A statistically significant difference was not found in enzyme activity of succinate dehydrogenase and lactate dehydrogenase. DISCUSSION: 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.
05-25-2006 12:33 AM
No, he was being intellectually lazy. As a medical professional, he should have consulted the relevant literature rather than tossing off his uninformed opinion. Even a public database such as pubmed yields HUNDREDS of studies.
Originally Posted by Umpire10589
05-25-2006 12:34 AM
Inflammation isn't a disease as far as i'm aware. Wouldn't Hepatitus be a disease and saying it doesn't prevent disease be along the lines of..Doesn't protect you from cirohsis of the liver, hepatitus etc?
Please pardon my spelling i r not smaert
Edit: that was a question
05-25-2006 12:37 AM
Journal of Clinical Gastroenterology 2003; 37(4):336-33
Silymarin Retards the Progression of Alcohol-Induced Hepatic Fibrosis in Baboons
Charles S. Lieber, MD, MACP; Maria A. Leo, MD; Qi Cao, MD, PhD; Chaoling Ren, MD; Leonore M. DeCarli, BA
Hepatoprotective effects of silymarin in patients with alcoholic liver disease are controversial. For strict control, this was assessed in non-human primates.
As stated elsewhere, the possible reason for the controversy is from inconsistent results in other studies which may have been from lack of control over dose and compliance. The key words with regard to this study are "strict control".
Twelve baboons were fed alcohol with or without silymarin for 3 years with a nutritionally adequate diet.
Silymarin opposed the alcohol-induced oxidative stress (assessed by plasma 4-hydroxynonenal) and the rise in liver lipids and circulating ALT. Alcohol also increased hepatic collagen type I by 50% over the 3 years with a significant rise in mRNA for [alpha]1 (I) procollagen, both prevented by silymarin. There were corresponding morphologic changes: at 36 months, 2 of 6 animals fed alcohol had cirrhosis and 2 septal fibrosis, with perivenular fibrosis in 2, whereas with alcohol + silymarin, there was only 1 cirrhosis and 1 septal fibrosis, with perivenular fibrosis in 2, and virtually no lesions in the remaining 2.
These results indicate a broad reaching beneficial effect of silymarin against the ravages of liver disease. It also states that the blood tests and biopsies were reliable predictors for the actual physical state of the livers after three years. The subjects with the worse blood test and biopsy results had the most damage.
Silymarin retards the development of alcohol-induced hepatic fibrosis in baboons, consistent with several positive clinical trials. The negative outcome observed in other trials possibly reflects poor compliance resulting in irregular or low silymarin intake. Thus, in view of the innocuity of silymarin, it might be advisable in future clinical studies to insure the controlled administration of sufficient amounts of silymarin.
This conclusion of this study is definite. Silymarin retards fibrosis.
05-25-2006 12:37 AM
This statement ("These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or PREVENT ANY DISEASE.") is STANDARD on ALL supplements in the US because of the way our laws are set up. If something is a "supplement" then it doesn't go to the FDA for regulatory approval. If you assert that a supplement is to be used to treat or prevent disease, then by definition the item is no longer a supplement, it is a "drug" subject to FDA approval and cannot be sold without FDA approval. This is why these supplements we take contain that disclaimer (to try and shield themselves from FDA regulation).
Originally Posted by Jayhawkk
Some supplements are utter crap, some are actually dangerous, but there are a bunch of them that have real science behind their efficacy and safety but are treated as "supplements" by the regulatory scheme in the USA. This guy needs to get another doctor.
05-25-2006 12:40 AM
Gotcha, I was asking about the disease part becuse he bolded it then directly related it to inflammation of the liver as if saying the two were the same...Or at least that's what I got out of it but you know how my world is one which I live in alone
05-25-2006 12:43 AM
946 pub med hits using search terms: n acetyl cysteine and liver
05-25-2006 12:46 AM
1330 pubmed hits using search terms: S-adenosylmethionine and liver
05-25-2006 12:47 AM
First off: I wasnt being lazy, I just didnt mention that I too went on Pub Med to verify.
Here is where the problem lies with the studies you guys mentioned:
First rebuttal is in regards to the study with rats, suggesting that silymarin protects the liver from disease as you suggest.
First and foremost, even if a study shows that a certain compound will protect a rat, that in NO WAY means it will help a human. The reasons rats are used to predict effigy of medicines on humans is due to the similaritys of the rat and human brain (particuarly the hypothalmus, which controls mood). However you cannot assume that even if the rats liver was protected, that it would do the same for a person. The study does not conclusivly say why those rats were okay. It was one study, that has not been repeated with the same result in any of the articles put in so far.
Also, these studies are in regards to Silymarin alone, not the pills. Nor do any of these studies mention doses adminastered, Even if you believe Silymarin would protect your liver, none of these studies suggest how much would be needed to protect a human liver from AAS, (before you even get into how much is being taken for how long, what type.)
What this comes down to is... If they actually have been proven medically to work, doctors would prescribe it. They dont.
05-25-2006 12:48 AM
What he said.
Originally Posted by yeahright
Believe it or not, our old pals at the FDA insist that diseases may only be treated by a drug. Oh really .......
IMHO - it seems clear that the medical community (at least in the US) does not regularly develop products or provide services that seek to treat or prevent disease. They merely treat the symptoms. This community also scoffs at non-traditional forms of treatment such as chiropractic manipulation, using instead methods such as drugs to relax the muscles (although in and of themselves, these drugs do nothing to treat the problem (only the symptom).
For example - take niacin. Ever wonder why niacin isn't "prescribed" by MDs for certain lipid conditions; despite the FACT that it lowers LDL, raises HDL and lowers triglycerides? Why would drug companies chose instead to develop drugs aimed at doing the same thing - although these drugs have far more side-effects.
Go ahead - guess why?
Niacin is a lowly supplement (thus an MD won't write a script for it). No script = no $$ to Eli Lilly and the like.
05-25-2006 12:54 AM
So basically you go from a raving loon to someone interpreting and analying PUBMED articles...Where do you live so I know that I should stay away from water towers and grassy knowles
05-25-2006 12:56 AM
You can type in whatever you want on PubMed, and than post expirements done on rats with Silymarin (only one ingrediant in the liver pills), or others that merely suggest they may work. But when it comes down to it, if they were shown to work, than doctors would use it for their own medicines. However they do not. I am also aware the FDA label is used for legal reasons, however it also means that they have not been required to be studied for human ingestion, and for the purposes I believe we are discussing them.
Last time I checked, alchohol (which a few of these "studies" are about, wasnt 17-alkaylated..... Last time I checked,rats dont take oral steroids... No one knows if this product works on humans, or if it does, how much needs to be taken, per individual case. If they did know this, like I said doctors would prescribe it.
And you say I am bad at arguing? Citing x number of hits on a cite you probably dont understand one word of means ****, as do all these articles you copied and pasted in my face. NOT ONE OF THEM has anything to do with steroid use and humans. Not one.
Also, inflamamation is a symptom of many liver diseases (cirohisis mainly). Put an article on here that says these pills (not one ingrediant), protect the liver from steroids in humans and ill drop out of school. I know you wont bc that article hasnt been written.
05-25-2006 12:59 AM
1: Clin Cancer Res. 2005 Dec 1;11(23):8441-8. Related Articles, Links
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Silibinin efficacy against human hepatocellular carcinoma.
Varghese L, Agarwal C, Tyagi A, Singh RP, Agarwal R.
Department of Pharmaceutical Sciences, School of Pharmacy and University of Colorado Cancer Center, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
PURPOSE: Hepatocellular carcinoma (HCC) is one of the most common recurrent malignancies, for which, currently, there is no effective therapy. Considering the antihepatotoxic activity of silibinin, a widely used drug and supplement for various liver disorders, together with its strong preventive and anticancer efficacy against various epithelial cancers, we investigated the efficacy of silibin against human HCC cells. EXPERIMENTAL DESIGN: Silibinin effects were examined on growth, cytotoxicity, apoptosis, and cell cycle progression in two different HCC cell lines, HepG2 (hepatitis B virus negative; p53 intact) and Hep3B (hepatitis B virus positive; p53 mutated). At molecular level, cell cycle effects of silibinin were assessed by immunoblotting and in-bead kinase assays. RESULTS: Silibinin strongly inhibited growth of both HepG2 and Hep3B cells with a relatively stronger cytotoxicity in Hep3B cells, which was associated with apoptosis induction. Silibinin also caused G1 arrest in HepG2 and both G1 and G2-M arrests in Hep3B cells. Mechanistic studies revealed that silibinin induces Kip1/p27 but decreases cyclin D1, cyclin D3, cyclin E, cyclin-dependent kinase (CDK)-2, and CDK4 levels in both cell lines. In Hep3B cells, silibinin also reduced the protein levels of G2-M regulators. Furthermore, silibinin strongly inhibited CDK2, CDK4, and CDC2 kinase activity in these HCC cells. CONCLUSION: Together, these results for the first time identify the biological efficacy of silibinin against HCC cells, suggesting the importance of conducting further investigations in preclinical HCC models, especially on in vivo efficacy, to support the clinical usefulness of silibinin against hepatocellular carcinoma in addition to its known clinical efficacy as an antihepatotoxic agent.
PMID: 16322307 [PubMed - indexed for MEDLINE]
05-25-2006 01:01 AM
When my liver values were through the roof my doctor told me to pick up some milk thistle from wal mart
05-25-2006 01:02 AM
1: Drug Metab Dispos. 2004 Jun;32(6):587-94. Related Articles, Links
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Silybin inactivates cytochromes P450 3A4 and 2C9 and inhibits major hepatic glucuronosyltransferases.
Sridar C, Goosen TC, Kent UM, Williams JA, Hollenberg PF.
Department of Pharmacology, The University of Michigan, Ann Arbor, MI 48109, USA.
Silybin, a major constituent of the milk thistle, is used to treat several liver disorders. Silybin inactivated purified, recombinant cytochromes P450 (P450) 3A4 and 2C9 in a mechanism-based manner. The inactivations were time-, concentration-, and NADPH-dependent. The inactivation of the 7-benzyloxy-4-(trifluoromethyl-)coumarin O-debenzylation activity (P450 3A4) was characterized by a K(I) of 32 microM, a k(inact) of 0.06 min(-1), and a t(1/2) of 14 min. Testosterone metabolism to 6-beta-hydroxytestosterone (P450 3A4) was also inactivated with a K(I) of 166 microM, a k(inact) of 0.08 min(-1), and a t(1/2) of 9 min. The 7-ethoxy-4-(trifluoromethyl)coumarin O-deethylation activity of purified human P450 2C9 was inactivated with a K(I) of 5 microM, a k(inact) of 0.14 min(-1), and a t(1/2) of 7 min. Parallel loss of heme was observed with both P450s. Activity of both P450 enzymes was not recovered after removal of silybin either by dialysis or by spin gel filtration. In addition, silybin inhibited the glucuronidation of 7-hydroxy-4-trifluoromethylcoumarin catalyzed by recombinant hepatic UDP-glucuronosyltransferases (UGTs) 1A1, 1A6, 1A9, 2B7, and 2B15, with IC(50) values of 1.4 microM, 28 microM, 20 microM, 92 microM, and 75 microM, respectively. Silybin was a potent inhibitor of UGT1A1 and was 14- and 20-fold more selective for UGT1A1 than for UGT1A9 and UGT1A6, respectively. Thus, careful administration of silybin with drugs primarily cleared by P450s 3A4 or 2C9 is advised, since drug-drug interactions cannot be excluded. The clinical significance of in vitro UGT1A1 inhibition is unknown.
PMID: 15155549 [PubMed - indexed for MEDLINE]
05-25-2006 01:03 AM
To test on rats?
Originally Posted by Jayhawkk
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