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Milk Thistle versus Liv.52

Favorite Liver Tonic

  • Milk Thistle

    Votes: 116 30.0%
  • Liv.52

    Votes: 212 54.8%
  • Other

    Votes: 59 15.2%

  • Total voters
    387

0o0o0o

Banned
Joined
Feb 27, 2009
Messages
212
Came Across This on another Thread, anyone have any good thoughts on the matter?-

Came accross this old thread because it comes up high on Google search for 'Milk Thistle versus Liv.52' So I thought it would be worth adding to the thread for anyone else who stumbles across it.

I've researched thoroughly both Milk Thistle and Liv.52. I realize this is a body builder forum. I've read all the posts here and read about 20+ clinical studies related to these subjects. Here's my conclusions for what they are worth:

1. Both Milk Thistle (or Sylmarin extract) and Liv.52 appear to have hepoprotective properties - they help protect your liver from damage.

2. Liv.52 is an Indian Herbal concoction consisting of serveral herbs none of which are Milk Thistle. Milk Thistle supplements do not have any of the herbs that Liv.52 does so they appear to be completely different supplements.

3. Liv.52 has much more 'hype' surrounding it. It's a brand. The primary clinical studies showing its benefit, especially the one that shows it is more effective than Milk Thistle were commissioned by the company that makes Liv.52. However there are other independent studies confirming it's efficacy.

4. There appears (in my research) to be more clinical studies from accredited, independent institutions regarding Milk Thistle and it's derivatives including Sylmarin extract and silybin phytosome (aka silybin Phosphatydilcholine). It's a generic herb, not a brand, like Liv.52.

5. In my judgement, probably the most effective supplement for liver protection would be one with silybin phytosome, sold under names like Maximum Milk Thistle and Siliphos. The reason is because the bioavailability of silybin phytosome is nearly 8 times that of regular Milk Thistle sylmarin extract. I believe if Liv.52 had any edge on Milk Thistle, it would be negated if not surpassed by silybin phytosome.

6. The conclusions of studies of Liv-52 are much more contradictory than Milk Thistle. One example is this study which states "Liv 52, an Ayurvedic hepatoprotective agent, is not useful in the management of alcohol-induced liver disease. "

Herbal medicines for liver diseases.

Where this study concludes "We conclude that Liv-52 possess hepatoprotective effect in cirrhotic patients. This protective effect of Liv-52 can be attributed to the diuretic, anti-inflammatory, anti-oxidative, and immunomodulating properties of the component herbs. "

ScienceDirect - Phytomedicine : The efficacy of Liv-52 on liver cirrhotic patients: A randomized, double-blind, placebo-controlled first approach

I find the contradictory evidence troublesome. While I still believe Liv.52 definitely has hepoprotective efficacy to some degree, I agree with the statement in one study which said "Standardization of herbal medicines has been a problem and prospective, randomized, placebo-controlled clinical trials are lacking to support their efficacy. The methodological qualities of clinical trials of treatment with herbal preparations are poor. "

7. I see a lot of that Liv.52 stuff being sold on E-bay for dirt cheap. Is it the real thing? How come drugstore.com or Rite Aid doesn't sell it? These things bring up yellow (not red) flags for me. Milk Thistle supplements are widely available just about anywhere.

8. It appears Liv.52 was withdrawn from the market at some point. This study in Nov 2004 stated "LIV.52 has been withdrawn from the market because of deleterious effects in patients with liver disease."

Use of herbal supplements for chronic liver diseas...[Clin Gastroenterol Hepatol. 2004] - PubMed Result

I'm not a doctor, just a reader. You can make your own decision. Based on the evidence I'd choose to take sylibin phytosome instead of Liv.52. It also has documented anti-cancer properties which is a bonus. Tons of articles to read on it here:

Milk Thistle Cancer: Health Information from Peer Reviewed Scientific Research Reports

Finally, I have one big question. In reading all the posts here, no matter what people are using, they saying something like "xxx works great for me."
 
Came Across This on another Thread, anyone have any good thoughts on the matter?-

Came accross this old thread because it comes up high on Google search for 'Milk Thistle versus Liv.52' So I thought it would be worth adding to the thread for anyone else who stumbles across it.

I've researched thoroughly both Milk Thistle and Liv.52. I realize this is a body builder forum. I've read all the posts here and read about 20+ clinical studies related to these subjects. Here's my conclusions for what they are worth:

1. Both Milk Thistle (or Sylmarin extract) and Liv.52 appear to have hepoprotective properties - they help protect your liver from damage.

2. Liv.52 is an Indian Herbal concoction consisting of serveral herbs none of which are Milk Thistle. Milk Thistle supplements do not have any of the herbs that Liv.52 does so they appear to be completely different supplements.

3. Liv.52 has much more 'hype' surrounding it. It's a brand. The primary clinical studies showing its benefit, especially the one that shows it is more effective than Milk Thistle were commissioned by the company that makes Liv.52. However there are other independent studies confirming it's efficacy.

4. There appears (in my research) to be more clinical studies from accredited, independent institutions regarding Milk Thistle and it's derivatives including Sylmarin extract and silybin phytosome (aka silybin Phosphatydilcholine). It's a generic herb, not a brand, like Liv.52.

5. In my judgement, probably the most effective supplement for liver protection would be one with silybin phytosome, sold under names like Maximum Milk Thistle and Siliphos. The reason is because the bioavailability of silybin phytosome is nearly 8 times that of regular Milk Thistle sylmarin extract. I believe if Liv.52 had any edge on Milk Thistle, it would be negated if not surpassed by silybin phytosome.

6. The conclusions of studies of Liv-52 are much more contradictory than Milk Thistle. One example is this study which states "Liv 52, an Ayurvedic hepatoprotective agent, is not useful in the management of alcohol-induced liver disease. "

Herbal medicines for liver diseases.

Where this study concludes "We conclude that Liv-52 possess hepatoprotective effect in cirrhotic patients. This protective effect of Liv-52 can be attributed to the diuretic, anti-inflammatory, anti-oxidative, and immunomodulating properties of the component herbs. "

ScienceDirect - Phytomedicine : The efficacy of Liv-52 on liver cirrhotic patients: A randomized, double-blind, placebo-controlled first approach

I find the contradictory evidence troublesome. While I still believe Liv.52 definitely has hepoprotective efficacy to some degree, I agree with the statement in one study which said "Standardization of herbal medicines has been a problem and prospective, randomized, placebo-controlled clinical trials are lacking to support their efficacy. The methodological qualities of clinical trials of treatment with herbal preparations are poor. "

7. I see a lot of that Liv.52 stuff being sold on E-bay for dirt cheap. Is it the real thing? How come drugstore.com or Rite Aid doesn't sell it? These things bring up yellow (not red) flags for me. Milk Thistle supplements are widely available just about anywhere.

8. It appears Liv.52 was withdrawn from the market at some point. This study in Nov 2004 stated "LIV.52 has been withdrawn from the market because of deleterious effects in patients with liver disease."

Use of herbal supplements for chronic liver diseas...[Clin Gastroenterol Hepatol. 2004] - PubMed Result

I'm not a doctor, just a reader. You can make your own decision. Based on the evidence I'd choose to take sylibin phytosome instead of Liv.52. It also has documented anti-cancer properties which is a bonus. Tons of articles to read on it here:

Milk Thistle Cancer: Health Information from Peer Reviewed Scientific Research Reports

Finally, I have one big question. In reading all the posts here, no matter what people are using, they saying something like "xxx works great for me."
I had to see my doctor after doing some orals in my cycle . I put stress on my liver from d-bol. I sent him the link to the studies for Liv-52 and asked him if I could take this while I heal up. He said not to. I read on my advisory section hospital website that they only recognize milk thistle for liver regeneration and to avoid other herbal medicines if you are being treated for liver disease. It states that the herbal medicines will do more damage than good if you take them to help healing.
 
I had to see my doctor after doing some orals in my cycle . I put stress on my liver from d-bol. I sent him the link to the studies for Liv-52 and asked him if I could take this while I heal up. He said not to. I read on my advisory section hospital website that they only recognize milk thistle for liver regeneration and to avoid other herbal medicines if you are being treated for liver disease. It states that the herbal medicines will do more damage than good if you take them to help healing.
Can you post a link to this "hospital website" please? Thanks.
 
I couldn't tell you which is better than the other...but I do take both. The reason it is so cheap on eBay is you're ordering it directly from India, which is dirt cheap. It takes a little while to arrive via India Post.

There are plenty of studies showing the many benefits of Liv52.

Liv52 has a newer product out called LiverCure...
 
N-Acetyl-Cysteine (NAC)
 
Liv52 has a newer product out called LiverCure...[/QUOTE]

That is totally incorrect if IP's Livercure is what you mean.

Livercure is a sulfa drug attached to an aspirin molecule.
It was originally used as an anti-inflam for Rheumatoid arthritis.

It somehow causes an enzyme cascade that reverses Hep C damage.

They discovered this use in England.

It kills all the probiotics in your upper and lower gut and you must
supplement probiotics or feel like shit. Not just some Yogurt either.
Buy good probio's or you will be sorry.

ANGEL
 
There are three main types of hepatotoxicity seen clinically from the use of oral steroids. These include intrahepatic cholestasis, peliosis hepatis, and hepatic adenoma. Cholestasis is the most common side effect seen, with peliosis and adenoma being much less common. Cholestasis occurs when bile flow through the liver is impaired. When this happens, products that are normally carried in the bile to the gut and excreted begin to build up within the liver. These products can reach toxic levels and cause cell damage and death. Monitoring for liver enzymes such as AST and ALT could detect if damage was occurring in the liver. Cholesterol metabolism becomes impaired as a result of cholestasis, with an increase in LDL (Bad cholesterol) and decrease in HDL (Good cholesterol).2 These cholesterol changes may lead to an increased risk of heart disease, and are very common with oral steroid use. HDL below 10ng/dl is not uncommon to hear about. That’s bad considering the desired level is greater than 40ng/dl! Finally, jaundice may occur. What essentially occurs is a buildup of bilirubin, which is formed when red blood cells break down. Since it cannot be excreted in the bile, it essentially backs up into the body and causes a yellowing of skin and eyes. This is not something you want to see!


Ursodeoxycholic acid (UDCA) is a chemical called a bile acid. It occurs naturally in bile and can be used to dissolve gallstones. The liver produces bile that is stored in the gall bladder. Bile is released by the gall bladder to aid the digestion of fats. It consists of cholesterol dissolved within bile salts. Gallstones occur in the gall bladder as a result of too much cholesterol, or too few bile salts within the bile. The imbalance causes excess cholesterol to separate out of the bile and form stones. Ursodeoxycholic acid causes gallstones to dissolve by a mechanism that is not fully understood. It is known to reduce the production of cholesterol by the liver and also to reduce the absorption of cholesterol from the gut. Both of these actions decrease the amount of cholesterol that passes into the bile. Also, since ursodeoxycholic acid is a bile acid itself, it increases the level of bile acids within the bile. The combination of these two factors reverses the imbalance and stops the cholesterol separating out of the bile. The gallstones then begin to dissolve.

Besides existing in its natural form, UDCA has been synthesized, and all pharmaceutical formulations are synthetic. Besides dissolving gallstones, UDCA exerts other actions of more interest to AAS using bodybuilders. Oral 17 alpha alkylated steroids often cause a condition called cholestasis. Cholestasis is any condition in which bile excretion from the liver is blocked, which can occur either in the liver where bile is formed, or in the bile ducts.

Extrahepatic cholestasis -- which occurs outside the liver -- can be caused by bile duct tumors, strictures, cysts, diverticula, and other damage. Other potential causes for this type include stones in the common bile duct, pancreatitis, pancreatic tumor or pseudocyst, primary sclerosing cholangitis, and compression due to a mass or tumor on a nearby organ.

Intrahepatic cholestasis -- which occurs inside the liver -- can be caused by sepsis (generalized infection), bacterial abscess, drugs, total parenteral nutrition (being fed intravenously), lymphoma, tuberculosis, sarcoidosis and amyloidosis. Other causes of this form of the disorder include primary biliary cirrhosis, primary sclerosing cholangitis, viral hepatitis (A,B,C, etc.), alcoholic liver disease, pregnancy, Sjogren's syndrome and others.

-Symptoms include the following: -Itching -Jaundiced (yellow) skin or eyes -Inability to digest certain foods -Nausea, vomiting -Right upper quadrant abdominal pain -Organ failure in cases of sepsis (but not from cholestasis itself) -Rash or fever in some cases of drug-induced cholestasis -Clay-colored or white stools -Dark urine

Often times a panel of standard liver function tests will show cholestasis before the symptoms even manifest themselves, but in general laboratory tests have limited diagnostic value. Transaminase (ALT, AST), alkaline phosphate, and bilirubin levels are typically elevated in proportion to the severity of the disease. AST and ALT can be elevated by exercise, so those are not particularly helpful in diagnosing cholestasis (1).

It is intrahepatic cholestasis caused by drugs (i.e.oral 17 alpha alkylated anabolic steroids) that is of greatest concern to bodybuilders. It has been proposed that oral steroids interfere with the pump that exports bile out of liver cells.

UDCA exerts a number of therapeutic effects which prevent and treat cholestasis. For instance, we mentioned the bile transport pump. UDCA has been shown to stimulate enzymes that increase the density of these bile transporters, allowing bile to exit the liver more readily (2,3). UDCA also protects hepatocytes (liver cells) against bile induced apoptosis (programmed cell death) (2).

Whatever the primary mechanism is for AAS induced cholestasis, UDCA has proven effective in treating the condition. Quoting from one study,

"A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae...Liver biopsy was compatible with cholestasis induced by anabolic steroids...The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. CONCLUSION: Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement. (4).

Interestingly, there seems to be a genetic disposition to the development of drug induced cholestasis (5). This may explain why only some oral AAS users develop the disease and others can endure heavy cycles of 17-alpha alkylated orals. Cholestasis as well as hepatitis caused by non 17-alpha alkylated injectable steroids has been reported, but is rare.

Cholestasis can be caused by estrogen as well, both synthetic and endogenous. It is not uncommon for cholestasis to develop during pregnancy, when estrogen levels are high. It’s possible the rare reported cases of testosterone induced cholestasis might be due to elevated estrogen levels in susceptible individuals.

It should be stressed that if one develops the symptoms of drug induced cholestasis, the first line of treatment is to immediately discontinue the drug, and begin treatment with UDCA. Although there are no studies showing UDCA exerts any prophylactic effects against AAS induced cholestasis, the proposed mechanism whereby it upregulates hepatic bile transporters suggests it may very well help prevent the disease by increasing bile flow out of the liver. Once the offending drug is withdrawn, and UDCA therapy begun, the disease typically resolves.

UDCA has also been shown to lower both total cholesterol and LDL (bad) cholesterol via at least two different mechanisms. In one study (6) researchers observed that UDCA lowered the hepatic (liver) production of cholesterol by interfering with a key enzyme in cholesterol synthesis.

In another study, UDCA was administered to animals with moderately elevated cholesterol, somewhat typical of what is seen in many people subsisting on high fat western diets (and typical of what is seen in oral AAS users). Here UDCA lowered plasma LDL by increasing the number of LDL binding sites on the liver, allowing for greater LDL uptake by the liver (7).

So we see an added health benefit to UDCA use, even in those AAS users who do not experience cholestasis. Most bodybuilders watch their fat intake, but on a high protein diet that includes red meat, UDCA might be a worthwhile supplement to consider if one is concerned about cholesterol (and who isn’t these days).

When bile enters the digestive tract, a certain portion is reabsorbed, leading to cholesterol reuptake. UDCA seems to block a portion of this cholesterol reuptake, providing for yet another mechanism whereby UDCA lowers cholesterol (8).

Dosages of commercial brands of UDCA vary depending on the type and severity of liver disease. For preventative purposes 500 mg per day might be sufficient. Once liver disease has developed, one ought to see their doctor, but a typical recommended dose is 13 to 15 mg/kg/day which may be given in 2 divided doses, i.e. in the morning and at bedtime, with food. But again, if any of the symptoms listed above develop, or liver tests come out showing cholestasis or some other liver disorder, don’t self medicate; see your doctor, and lay off the orals.
 
Liv52 has a newer product out called LiverCure...
That is totally incorrect if IP's Livercure is what you mean.

Livercure is a sulfa drug attached to an aspirin molecule.
It was originally used as an anti-inflam for Rheumatoid arthritis.ANGEL[/QUOTE]

Angel...sorry, but I must correct you, here is the version of LiverCare that I am speaking of, and it is from the makers of Liv52, not the same product that you tried to correct me on.

http://www.ayurvedicherbsdirect.com/livercare-himalaya-p-60.html?gclid=CPWqjZ_e_5oCFSQeDQodD3gbfA

That being said, this could be Liv52 repackaged. I read in a thread somewhere here on PM, that this product is Liv52 reformulated.
 
Angel...sorry, but I must correct you, here is the version of LiverCare that I am speaking of, and it is from the makers of Liv52, not the same product that you tried to correct me on.

http://www.ayurvedicherbsdirect.com/livercare-himalaya-p-60.html?gclid=CPWqjZ_e_5oCFSQeDQodD3gbfA

That being said, this could be Liv52 repackaged. I read in a thread somewhere here on PM, that this product is Liv52 reformulated.

He probably corrected you because you called it LiverCure and not LiverCare
 
I had to see my doctor after doing some orals in my cycle . I put stress on my liver from d-bol. I sent him the link to the studies for Liv-52 and asked him if I could take this while I heal up. He said not to. I read on my advisory section hospital website that they only recognize milk thistle for liver regeneration and to avoid other herbal medicines if you are being treated for liver disease. It states that the herbal medicines will do more damage than good if you take them to help healing.

This is the only 100% pharmaceutical grade Silmarin (Milkthistle) on the market www.carsil.com
 
I had to see my doctor after doing some orals in my cycle . I put stress on my liver from d-bol. I sent him the link to the studies for Liv-52 and asked him if I could take this while I heal up. He said not to. I read on my advisory section hospital website that they only recognize milk thistle for liver regeneration and to avoid other herbal medicines if you are being treated for liver disease. It states that the herbal medicines will do more damage than good if you take them to help healing.

When I had elevated liver enzymes my Dr. said the exact same thing regarding the use of milk thistle.
 
There are three main types of hepatotoxicity seen clinically from the use of oral steroids. These include intrahepatic cholestasis, peliosis hepatis, and hepatic adenoma. Cholestasis is the most common side effect seen, with peliosis and adenoma being much less common. Cholestasis occurs when bile flow through the liver is impaired. When this happens, products that are normally carried in the bile to the gut and excreted begin to build up within the liver. These products can reach toxic levels and cause cell damage and death. Monitoring for liver enzymes such as AST and ALT could detect if damage was occurring in the liver. Cholesterol metabolism becomes impaired as a result of cholestasis, with an increase in LDL (Bad cholesterol) and decrease in HDL (Good cholesterol).2 These cholesterol changes may lead to an increased risk of heart disease, and are very common with oral steroid use. HDL below 10ng/dl is not uncommon to hear about. That’s bad considering the desired level is greater than 40ng/dl! Finally, jaundice may occur. What essentially occurs is a buildup of bilirubin, which is formed when red blood cells break down. Since it cannot be excreted in the bile, it essentially backs up into the body and causes a yellowing of skin and eyes. This is not something you want to see!


Ursodeoxycholic acid (UDCA) is a chemical called a bile acid. It occurs naturally in bile and can be used to dissolve gallstones. The liver produces bile that is stored in the gall bladder. Bile is released by the gall bladder to aid the digestion of fats. It consists of cholesterol dissolved within bile salts. Gallstones occur in the gall bladder as a result of too much cholesterol, or too few bile salts within the bile. The imbalance causes excess cholesterol to separate out of the bile and form stones. Ursodeoxycholic acid causes gallstones to dissolve by a mechanism that is not fully understood. It is known to reduce the production of cholesterol by the liver and also to reduce the absorption of cholesterol from the gut. Both of these actions decrease the amount of cholesterol that passes into the bile. Also, since ursodeoxycholic acid is a bile acid itself, it increases the level of bile acids within the bile. The combination of these two factors reverses the imbalance and stops the cholesterol separating out of the bile. The gallstones then begin to dissolve.

Besides existing in its natural form, UDCA has been synthesized, and all pharmaceutical formulations are synthetic. Besides dissolving gallstones, UDCA exerts other actions of more interest to AAS using bodybuilders. Oral 17 alpha alkylated steroids often cause a condition called cholestasis. Cholestasis is any condition in which bile excretion from the liver is blocked, which can occur either in the liver where bile is formed, or in the bile ducts.

Extrahepatic cholestasis -- which occurs outside the liver -- can be caused by bile duct tumors, strictures, cysts, diverticula, and other damage. Other potential causes for this type include stones in the common bile duct, pancreatitis, pancreatic tumor or pseudocyst, primary sclerosing cholangitis, and compression due to a mass or tumor on a nearby organ.

Intrahepatic cholestasis -- which occurs inside the liver -- can be caused by sepsis (generalized infection), bacterial abscess, drugs, total parenteral nutrition (being fed intravenously), lymphoma, tuberculosis, sarcoidosis and amyloidosis. Other causes of this form of the disorder include primary biliary cirrhosis, primary sclerosing cholangitis, viral hepatitis (A,B,C, etc.), alcoholic liver disease, pregnancy, Sjogren's syndrome and others.

-Symptoms include the following: -Itching -Jaundiced (yellow) skin or eyes -Inability to digest certain foods -Nausea, vomiting -Right upper quadrant abdominal pain -Organ failure in cases of sepsis (but not from cholestasis itself) -Rash or fever in some cases of drug-induced cholestasis -Clay-colored or white stools -Dark urine

Often times a panel of standard liver function tests will show cholestasis before the symptoms even manifest themselves, but in general laboratory tests have limited diagnostic value. Transaminase (ALT, AST), alkaline phosphate, and bilirubin levels are typically elevated in proportion to the severity of the disease. AST and ALT can be elevated by exercise, so those are not particularly helpful in diagnosing cholestasis (1).

It is intrahepatic cholestasis caused by drugs (i.e.oral 17 alpha alkylated anabolic steroids) that is of greatest concern to bodybuilders. It has been proposed that oral steroids interfere with the pump that exports bile out of liver cells.

UDCA exerts a number of therapeutic effects which prevent and treat cholestasis. For instance, we mentioned the bile transport pump. UDCA has been shown to stimulate enzymes that increase the density of these bile transporters, allowing bile to exit the liver more readily (2,3). UDCA also protects hepatocytes (liver cells) against bile induced apoptosis (programmed cell death) (2).

Whatever the primary mechanism is for AAS induced cholestasis, UDCA has proven effective in treating the condition. Quoting from one study,

"A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae...Liver biopsy was compatible with cholestasis induced by anabolic steroids...The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. CONCLUSION: Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement. (4).

Interestingly, there seems to be a genetic disposition to the development of drug induced cholestasis (5). This may explain why only some oral AAS users develop the disease and others can endure heavy cycles of 17-alpha alkylated orals. Cholestasis as well as hepatitis caused by non 17-alpha alkylated injectable steroids has been reported, but is rare.

Cholestasis can be caused by estrogen as well, both synthetic and endogenous. It is not uncommon for cholestasis to develop during pregnancy, when estrogen levels are high. It’s possible the rare reported cases of testosterone induced cholestasis might be due to elevated estrogen levels in susceptible individuals.

It should be stressed that if one develops the symptoms of drug induced cholestasis, the first line of treatment is to immediately discontinue the drug, and begin treatment with UDCA. Although there are no studies showing UDCA exerts any prophylactic effects against AAS induced cholestasis, the proposed mechanism whereby it upregulates hepatic bile transporters suggests it may very well help prevent the disease by increasing bile flow out of the liver. Once the offending drug is withdrawn, and UDCA therapy begun, the disease typically resolves.

UDCA has also been shown to lower both total cholesterol and LDL (bad) cholesterol via at least two different mechanisms. In one study (6) researchers observed that UDCA lowered the hepatic (liver) production of cholesterol by interfering with a key enzyme in cholesterol synthesis.

In another study, UDCA was administered to animals with moderately elevated cholesterol, somewhat typical of what is seen in many people subsisting on high fat western diets (and typical of what is seen in oral AAS users). Here UDCA lowered plasma LDL by increasing the number of LDL binding sites on the liver, allowing for greater LDL uptake by the liver (7).

So we see an added health benefit to UDCA use, even in those AAS users who do not experience cholestasis. Most bodybuilders watch their fat intake, but on a high protein diet that includes red meat, UDCA might be a worthwhile supplement to consider if one is concerned about cholesterol (and who isn’t these days).

When bile enters the digestive tract, a certain portion is reabsorbed, leading to cholesterol reuptake. UDCA seems to block a portion of this cholesterol reuptake, providing for yet another mechanism whereby UDCA lowers cholesterol (8).

Dosages of commercial brands of UDCA vary depending on the type and severity of liver disease. For preventative purposes 500 mg per day might be sufficient. Once liver disease has developed, one ought to see their doctor, but a typical recommended dose is 13 to 15 mg/kg/day which may be given in 2 divided doses, i.e. in the morning and at bedtime, with food. But again, if any of the symptoms listed above develop, or liver tests come out showing cholestasis or some other liver disorder, don’t self medicate; see your doctor, and lay off the orals.

good info man!
 
So is Milk Thistle or LIV-52 in the running lead here?
 
Does anyone actually have any before and after liver value results to back their opinions up??

Id love some actual numbers. I need to get one of these products going in my daily routine
 
its a pretty close race so far really, it was in mt but now its liv 52

you don't have to use one or the other-- you should be taking both

here is a very good liver dextox for those who have elevated LFT's from gear/drugs

NAC-- 600mg 2'xs day (make sure to use aprx 1 gram Vit-C to 600mg NAC)

Liv-52- 2 tabs 2-3 X's day (depending on how severe the liver strain)

Milk thistle- 500-1000mg 2 x's day

ALA is good too- I like to use a product that supplies 300mg ALA with 500mg ALCAR per pill for overall health benefits (do this 2'x day)
 
you don't have to use one or the other-- you should be taking both

here is a very good liver dextox for those who have elevated LFT's from gear/drugs

NAC-- 600mg 2'xs day (make sure to use aprx 1 gram Vit-C to 600mg NAC)

Liv-52- 2 tabs 2-3 X's day (depending on how severe the liver strain)

Milk thistle- 500-1000mg 2 x's day

ALA is good too- I like to use a product that supplies 300mg ALA with 500mg ALCAR per pill for overall health benefits (do this 2'x day)

If you have to take 500-1000mg 2x`s Milk thisle per day, that tells me that the Milk thisle is very low grade, if the Milk thisle is pure 100% grade,you will need only 70-100mg per day.
 
I have personal experience with URSO 250mg. My doctor ordered a LFT Panel blood work . I had elevated ALT/AST levels (400 range) and buildup of bilirubin in my body (4.0 range). Prescribed Urso 250MG 3 times a day. Levels drop to (175 ALT/AST range) (bilirubin 1.2 range).
 
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