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
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. [email protected]
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
05-25-2006, 12:46 AM
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
Click here to read
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
05-25-2006, 01:03 AM
A raving loon??? Please if you want to knock me on something I say, go ahead... I can take your punches. But dont start making this personal. I wrote this thread for the same reason people responded to mine: to help. I did it bc I was so grateful of all the help you guys gave me, that I wanted to give back somehow. I know nothing about AAS compared to you guys, I know this and I want to learn in the future. I do know a thing or two about the ingrediants on the liver bottle, and the terminology being used in these studies. I do not want to get you guys mad, thats the last thing I want. But please just dont throw out what I say on liver protection because I dont know something else.
05-25-2006, 01:06 AM
The last study actually ends with the concession that the study drew no conclusions... Thats what Im saying.
05-25-2006, 01:07 AM
I am going to bed though bc I have a midterm at 8 am.... I am new to this board and I see I have red bars... I assume this is bad
05-25-2006, 01:13 AM
Not from me, and I wouldn't be concerned. The point is, we are here to learn. If forum members didn't care, we would just be like everyone else.
Boy - I'm going back to merely making foolish comments. It is a lot easier.
05-25-2006, 01:15 AM
Its ok... I really dont care if I have red stuff or green, I just want to learn, and help people, which is what I tried to do... But about what I want to know, you guys are the knowledgable ones, not me, so I will stop posting trying to be helpful stuff for now.
05-25-2006, 01:16 AM
Wasn't from me either and most of my comments are in jest and harmless don't take them personal...That being said, my doctor did tell me to pick some up to help lower the levels of course i'll also say that she also thought taking in 75 grams of whey a day was the culprit :P
05-25-2006, 01:20 AM
Originally Posted by Umpire10589
Ahhhhhh, but the abstract begins by citing silybin as an accepted treatment for several liver disorders.
You started out by saying "these are the worst kind of snake oil, my dad doesn't believe in them, my doc doesn't." This was inflamatory and predicated upon logic errors.
Now, you've refined your point downwards to something kinda reasonable.
If your point is that "the hepaprotective effects users are analogizing" may not be what we expect.....then point taken.
Just because milk thistle is used to treat (as a prescription medicine) alcoholic liver disease in europe, doesn't necessarily mean that it can protect from the damage done by oral steroids. The same goes for Sam-E, alpha lipoic acid, n acytl cysteine, etc. Each of these components have been demonstrated to have efficacy in the protection of the liver from toxic assault under certain circumstances, and in some instances in the repair of liver damage (sam-e has some evidence of being able to reverse cirrosis). In utilizing these for our purposes, we are drawing analogies which in the end could turn out to be flawed but that's a world away from calling these snake oil without any evidence to support their use.
Last edited by yeahright; 05-25-2006 at 02:08 AM.
05-25-2006, 01:45 AM
05-25-2006, 02:38 AM
I think that at most what we can say that these natural supplements ability to protect HUMAN liver specifically from oral AAS, needs more research. But just because the FDA doesnt approve something as a prescription drug for the purpose of treating a specific medical condition is NOT sufficient proof that it DOES NOT help with that condition.
It should be no secret by now that in the past (including recent past) there have been inexpensive natural compounds that were shown to effectively treat a known medical condition in multiple studies, only to have their efficacy shot down by the FDA on some technicality. Does that prove that compound definately DOES or definately DOES NOT help? Not neccesarily. BUT.......In my mind it the only thing it proves is that at least SOME members of the FDA are applying a double standard to different compounds. For instance green tea has a few studies fitting the FDA's rigid criteria for a "legitimate study", that showed statistically significant benefits against cancer. The FDA dug deep to find an excuse why the studies were not valid. (btw, the standard for studies according to the FDA isnt really an extesively HIGH standard as it is an extensively SPECIFIC standard.) That way they were able to justify the dismisal of a couple of the studies that used various DOSES of green tea in subjects even though the curve obviously pointed towards more benefit w/ more green tea. And the remaining studies wich DID meet their criteria (wich basically consists of group A doesnt take any, and group B takes x ammount of cups of green tea per day.) They still denied it's effectiveness based on the fact that the studies that met their rigid criteria showed a DIFFERENT PERCENTAGE of subjects benefiting than the other studies w/ similar criteria. The FDA then stated flatly.... "It is unlikely that green tea is beneficial for treating or preventing prostate cancer." All because of a DIFFERENT PERCENTAGE. Even though all the studies used in the meta-analysis DID SHOW AN OVERWHELMING MAJORITY OF SUBJECTS DID BENEFIT FROM THE GREEN TEA SUPPLEMENTATION.
So basically by their study standards, one study could (hypothetically) use 10 cups of green tea for the B group and zero in the control group, and conclude that it showed a 52% reduction in prostate cancer. Then the next study could use 20 cups of green tea per day for the Green tea group, and show a 73% reduction, and by the logic the FDA spokesman applied to the topic, the studies would show to big of a difference in the percentage of beneficiaries therefore green tea doesnt work.
You see how easy it is to make numbers appear to mean what someone wants them to mean.
On the other side of the coin, there was a doctor that worked for the FDA who decided to be a "whistle blower" and alleged that some members of the FDA new full well the danger of the now nearly infamous "Vioxx" and approved it ANYWAY (possibly for kick backs from big pharma) so the pharm company wouldnt have wasted all that research money and could "Win back" some of that money w/ a quick couple hundred million dollars before people start dying and then they would have it pulled and play dumb about it.
THAT is why I dont consider what the FDA approves or doesnt approve for medical treatment to be the be all end all of weather something can be a valid treatment for something. The medical industry is a bussiness. THere are alot of good hearted people that want to cure diseases and help people, but they arent always the ones that get to decide what drugs or supps get approved and what conditions the doctors are "allowed" to prescribe them for. (without being liable).
That being said, allthough I believe there are flaws w/ the system, I do think it's important that we have regulating bodies LIKE the FDA. But the system is only effective when the key players are functioning for THE GREATER GOOD OF THE WHOLE. And not just the greater financial good. I mean lets face it....... Green Tea is alot simpler, cheaper and more pleasant than oohhhhh lets say ummmmm CHEMO THERAPY.
Can it be used reliably and effectively? For that matter can alleged herbal liver detoxifiers be used reliably and effectively?
Until everybody (including EVERYONE in the FDA) is pushing for the greater good of the patients (and not some fat cat's bank account) we wont even see sufficient studies being done to know for sure if they are and/or to what extent.................Unicron Spawn:bb:
05-25-2006, 06:29 AM
Just an FYI brother. Hepatitis=inflammation of liver. "-itis"=inflammation. Example: Diverticulitis=inflammation of diverticula, pericarditis=inflammation of the pericardium...Originally Posted by Jayhawkk
Give a man a fish, feed him for a day. Teach a man to fish, feed him for life. Lao Tse 6th century BC
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