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TUDCA or UDCA?

A few words on the hepatotoxicity of 17a-methylated androgens/anabolics

1. 17a-methylated androgens/anabolics are hepatotoxic.
The liver toxicity of steroids is an under-researched field, but there seems to be a strong correlation between how easily the body can metabolize a steroid & its toxicity. Metribolone -- a truly excessively toxic compound -- is often referred to in the literature as a 'non-metabolizable androgen'. (1, 2, 3, etc.) Mibolerone, another deadly-toxic anabolic steroid, is also effectively 'non-metabolizable': The main metabolite of mibolerone in humans is... unchanged mibolerone. And by a very wide margin.

Methylstenbolone, which is resistant to 17b-HSD and 3b-HSD, is obviously difficult for the body to clear. It should therefore be no safer, no less toxic, than Superdrol or M1T -- compounds which share very similar traits.

2. Liver injury due to oral anabolic use typically manifests itself as cholestasis.
Hepatotoxicity induced by oral anabolic compounds tends to be characterized by enlargement of periportal hepatocytes, impairment of bile flow & dramatically increased serum levels of AST, ALT and GGT. In other words, cholestasis... but let's examine this a little bit further.

The word "cholestasis" gets thrown around a lot, but it can mean two very different things: The physical obstruction of hepatic bile flow -or- the impairment of bile secretion. In the former case, there is a mechanical block in the bile duct system; in the latter, bile is held in hepatocytes or cholangiocytes as it cannot be secreted. In both cases, what happens thereafter is that the retained hydrophobic bile salts -- which are strongly cytotoxic -- lead to cellular injury, then apoptosis, then necrosis, often followed by an inflammatory reaction and tissue fibrosis. This tissue damage, if advanced enough, can physically destroy bile ducts, worsening the condition.

The obstruction of bile flow is typically not something you'd experience after exposure to any toxin; it is the almost exclusive domain of inherited or autoimmune diseases which leave fibrotic lesions or scar-tissue in the liver, such as cystic fibrosis, primary biliary cirrhosis, and so on. Exposure to oral anabolic compounds can, however, result in the second form of cholestasis -- bile retention in hepatocytes -- thus the enlarged hepatocytes observed after their use.

3. There are three fundamental ways of preventing/treating cholestasis:


  1. Metabolic induction of hydrophobic bile acid detoxification
  2. Stimulation of impaired bile secretion
  3. Protection of hepatocytes from the toxic effects of hydrophobic bile acids and/or inhibition of hepatocyte apoptosis.

Cholestatic liver damage is caused by bile acid accumulation... But not all bile acids are toxic. Generally speaking, the fewer hydroxyl groups they bear, the more hydrophobic and cytotoxic they are. Hence lithocholic acid is markedly cytotoxic, deoxycholic acid is very slightly cytotoxic, and cholic acid is essentially non-cytotoxic. Treatment #1 would involve hastening the metabolic conversion of the more toxic bile acids to hydrophilic, less toxic compounds --- or increasing the synthesis of hydrophilic bile acids from cholesterol, which would decrease the cytotoxicity of the entire bile pool as a whole. This can seemingly be achieved with the oral administration of ursodeoxycholic acid (UDCA), which has been reported to activate the PXR/SXR nuclear receptor in hepatocytes, which then activates bile acid?metabolizing enzymes. It is reasonable to assume that Tauroursodeoxycholic acid (TUDCA), the taurine conjugate of UDCA, should have the same effect.

As for #2... Bile secretion at the level of the hepatocyte is carried out by a group of transporter proteins: The bile salt export pump (BSEP), the phospholipid export pump (MDR3), the canalicular bilirubin conjugate export pump (MRP2), and a chloride-bicarbonate anion exchanger (AE2) for bicarbonate excretion. BSEP is the driving factor behind bile-acid dependent secretion, and MRP2/AE2 are the major forces behind bile-acid-independent bile secretion. Hydrophilic bile acids such as UDCA & TUDCA (and even, partially, cholic acid) have been shown to increase expression of BSEP mRNA; they activate BSEP coactivators by binding to the Farnesoid X Receptor (the "bile acid receptor"); they phosphorylate the BSEP protein via a Ca+/PKCa-mediated mechanism; lastly, they stimulate Cl -/HCO3 - exchange via this same PKCa induction, thus increasing AE2 levels.

Taken together, the above effects drastically enhance secretion of potentially toxic bile acids.

#3 can be complicated, but I will explain briefly: Certain toxic bile salts activate the Fas Death Receptor on hepatocytes. This leads to a cascade of dozens of protein interactions & ultimately to cell death. TUDCA, UDCA, and certain other compounds can diminish Fas?induced apoptosis, but, as far as I am aware, the exact mechanism is not known at this time. Fas activation here is not ligand-dependent, so the 'obvious' mechanism is out the window. The mechanism could, however, involve activation of the EGFR, which activates MAPK & the MAPK-mediated 'survival pathway' in hepatocytes; it might also involve inhibition, somewhere along the line, of the proapoptotic proteins Bax and Bid.

4. Recommendations
I strongly recommend TUDCA or UDCA to anybody considering a cycle containing oral androgens, for what should by now be obvious reasons. They are extremely potent at preventing or reversing 17aa-androgen-mediated liver damage. There's really no excuse not to take them, in my opinion, and I would advise you not to run a cycle if you can't afford them. Oral androgens can send you straight to the ER if the right precautions are not taken, & your health is much more important than a few more pounds of here-today-gone-tomorrow muscle.

Silymarin and silybin, the milk thistle extracts, are very strong antioxidants and free-radical scavengers in hepatic tissue. They impede hepatic lipid peroxidation, increase glutathione concentrations, and even have anti-inflammatory and tissue-regenerative properties... Other plant-extracted compounds, such as celastrol, have similar effects... But while these extracts are excellent to take for general liver health, they are weak protection and not an appropriate treatment for cholestasis, as they do not appear to impact bile acid secretion/metabolism at pharmacologically-relevant doses. Silymarin did increase bile secretion and improve bile acid metabolism in rats -- but that effect was primarily noticed at a dose of 100mg/kg, administered via i.p. injection (100% bioavailability), and therefore doesn't have much bearing on humans who take much smaller amounts orally (~10% bioavailability).

...But Primordial Performance's "Liver Juice" is silymarin/silybin attached to an excellent delivery complex, and should be quite effective if taken 3x/day. It is the best milk thistle supplement out there, in my opinion.

NAC is also a fine antioxidant and glutathione-booster, but it suffers from poor bioavailability & is usually very underdosed in commercially-available supplements... So I wouldn't bother with it.

Sanofi-Aventi (or is it just 'Sanofi' these days?) manufactures the popular phospholipid-complex product "Essentiale" and "Essentiale Forte". The phosphatidylcholine therein has been shown to help protect hepatic cell membranes against the damaging effects of chenodeoxycholic acid, can inhibit lipid peroxidation, and can induce cytochrome P450, which stimulates the metabolic clearance of bile acids... So there's a reason that it's the most popular OTC liver support in Europe and Asia... But "Essentiale" can be hard to find in the USA -- and, on its own, I don't believe that it is totally adequate protection for users of oral androgens.

And Liv-52? Mostly a waste of money. A blend of mild antioxidants is all there is to it.

The bottom line here is this: Oral anabolics/androgens are hepatotoxic. Period. If you are going to use them, I implore you to take sensible precautions. Antaeus shall release a novel and powerful liver-support product in the very near future. In the meantime, there's Thermolife's "Liver Longer" and Primordial's "Liver Juice". Both are cheap enough that there's no excuse not to take them.

-Jake
 
Curt James said:
A few words on the hepatotoxicity of 17a-methylated androgens/anabolics

1. 17a-methylated androgens/anabolics are hepatotoxic.
The liver toxicity of steroids is an under-researched field, but there seems to be a strong correlation between how easily the body can metabolize a steroid & its toxicity. Metribolone -- a truly excessively toxic compound -- is often referred to in the literature as a 'non-metabolizable androgen'. (1, 2, 3, etc.) Mibolerone, another deadly-toxic anabolic steroid, is also effectively 'non-metabolizable': The main metabolite of mibolerone in humans is... unchanged mibolerone. And by a very wide margin.

Methylstenbolone, which is resistant to 17b-HSD and 3b-HSD, is obviously difficult for the body to clear. It should therefore be no safer, no less toxic, than Superdrol or M1T -- compounds which share very similar traits.

2. Liver injury due to oral anabolic use typically manifests itself as cholestasis.
Hepatotoxicity induced by oral anabolic compounds tends to be characterized by enlargement of periportal hepatocytes, impairment of bile flow & dramatically increased serum levels of AST, ALT and GGT. In other words, cholestasis... but let's examine this a little bit further.

The word "cholestasis" gets thrown around a lot, but it can mean two very different things: The physical obstruction of hepatic bile flow -or- the impairment of bile secretion. In the former case, there is a mechanical block in the bile duct system; in the latter, bile is held in hepatocytes or cholangiocytes as it cannot be secreted. In both cases, what happens thereafter is that the retained hydrophobic bile salts -- which are strongly cytotoxic -- lead to cellular injury, then apoptosis, then necrosis, often followed by an inflammatory reaction and tissue fibrosis. This tissue damage, if advanced enough, can physically destroy bile ducts, worsening the condition.

The obstruction of bile flow is typically not something you'd experience after exposure to any toxin; it is the almost exclusive domain of inherited or autoimmune diseases which leave fibrotic lesions or scar-tissue in the liver, such as cystic fibrosis, primary biliary cirrhosis, and so on. Exposure to oral anabolic compounds can, however, result in the second form of cholestasis -- bile retention in hepatocytes -- thus the enlarged hepatocytes observed after their use.

3. There are three fundamental ways of preventing/treating cholestasis:


  1. Metabolic induction of hydrophobic bile acid detoxification
  2. Stimulation of impaired bile secretion
  3. Protection of hepatocytes from the toxic effects of hydrophobic bile acids and/or inhibition of hepatocyte apoptosis.

Cholestatic liver damage is caused by bile acid accumulation... But not all bile acids are toxic. Generally speaking, the fewer hydroxyl groups they bear, the more hydrophobic and cytotoxic they are. Hence lithocholic acid is markedly cytotoxic, deoxycholic acid is very slightly cytotoxic, and cholic acid is essentially non-cytotoxic. Treatment #1 would involve hastening the metabolic conversion of the more toxic bile acids to hydrophilic, less toxic compounds --- or increasing the synthesis of hydrophilic bile acids from cholesterol, which would decrease the cytotoxicity of the entire bile pool as a whole. This can seemingly be achieved with the oral administration of ursodeoxycholic acid (UDCA), which has been reported to activate the PXR/SXR nuclear receptor in hepatocytes, which then activates bile acid?metabolizing enzymes. It is reasonable to assume that Tauroursodeoxycholic acid (TUDCA), the taurine conjugate of UDCA, should have the same effect.

As for #2... Bile secretion at the level of the hepatocyte is carried out by a group of transporter proteins: The bile salt export pump (BSEP), the phospholipid export pump (MDR3), the canalicular bilirubin conjugate export pump (MRP2), and a chloride-bicarbonate anion exchanger (AE2) for bicarbonate excretion. BSEP is the driving factor behind bile-acid dependent secretion, and MRP2/AE2 are the major forces behind bile-acid-independent bile secretion. Hydrophilic bile acids such as UDCA & TUDCA (and even, partially, cholic acid) have been shown to increase expression of BSEP mRNA; they activate BSEP coactivators by binding to the Farnesoid X Receptor (the "bile acid receptor"); they phosphorylate the BSEP protein via a Ca+/PKCa-mediated mechanism; lastly, they stimulate Cl -/HCO3 - exchange via this same PKCa induction, thus increasing AE2 levels.

Taken together, the above effects drastically enhance secretion of potentially toxic bile acids.

#3 can be complicated, but I will explain briefly: Certain toxic bile salts activate the Fas Death Receptor on hepatocytes. This leads to a cascade of dozens of protein interactions & ultimately to cell death. TUDCA, UDCA, and certain other compounds can diminish Fas?induced apoptosis, but, as far as I am aware, the exact mechanism is not known at this time. Fas activation here is not ligand-dependent, so the 'obvious' mechanism is out the window. The mechanism could, however, involve activation of the EGFR, which activates MAPK & the MAPK-mediated 'survival pathway' in hepatocytes; it might also involve inhibition, somewhere along the line, of the proapoptotic proteins Bax and Bid.

4. Recommendations
I strongly recommend TUDCA or UDCA to anybody considering a cycle containing oral androgens, for what should by now be obvious reasons. They are extremely potent at preventing or reversing 17aa-androgen-mediated liver damage. There's really no excuse not to take them, in my opinion, and I would advise you not to run a cycle if you can't afford them. Oral androgens can send you straight to the ER if the right precautions are not taken, & your health is much more important than a few more pounds of here-today-gone-tomorrow muscle.

Silymarin and silybin, the milk thistle extracts, are very strong antioxidants and free-radical scavengers in hepatic tissue. They impede hepatic lipid peroxidation, increase glutathione concentrations, and even have anti-inflammatory and tissue-regenerative properties... Other plant-extracted compounds, such as celastrol, have similar effects... But while these extracts are excellent to take for general liver health, they are weak protection and not an appropriate treatment for cholestasis, as they do not appear to impact bile acid secretion/metabolism at pharmacologically-relevant doses. Silymarin did increase bile secretion and improve bile acid metabolism in rats -- but that effect was primarily noticed at a dose of 100mg/kg, administered via i.p. injection (100% bioavailability), and therefore doesn't have much bearing on humans who take much smaller amounts orally (~10% bioavailability).

...But Primordial Performance's "Liver Juice" is silymarin/silybin attached to an excellent delivery complex, and should be quite effective if taken 3x/day. It is the best milk thistle supplement out there, in my opinion.

NAC is also a fine antioxidant and glutathione-booster, but it suffers from poor bioavailability & is usually very underdosed in commercially-available supplements... So I wouldn't bother with it.

Sanofi-Aventi (or is it just 'Sanofi' these days?) manufactures the popular phospholipid-complex product "Essentiale" and "Essentiale Forte". The phosphatidylcholine therein has been shown to help protect hepatic cell membranes against the damaging effects of chenodeoxycholic acid, can inhibit lipid peroxidation, and can induce cytochrome P450, which stimulates the metabolic clearance of bile acids... So there's a reason that it's the most popular OTC liver support in Europe and Asia... But "Essentiale" can be hard to find in the USA -- and, on its own, I don't believe that it is totally adequate protection for users of oral androgens.

And Liv-52? Mostly a waste of money. A blend of mild antioxidants is all there is to it.

The bottom line here is this: Oral anabolics/androgens are hepatotoxic. Period. If you are going to use them, I implore you to take sensible precautions. Antaeus shall release a novel and powerful liver-support product in the very near future. In the meantime, there's Thermolife's "Liver Longer" and Primordial's "Liver Juice". Both are cheap enough that there's no excuse not to take them.

-Jake
Click to expand...
great post
 
And Liv-52? Mostly a waste of money. A blend of mild antioxidants is all there is to it.

so it's better to take blend of antioxidants and which am on it ASAP lol
 
I was looking into this a while ago and found this posted on another forum:



Before we talk about this amazing substance, let?s talk about what prompts its necessity in our research at all. Hepatoxicity, or liver toxicity, is often associated with administration of oral preparations/medications. This is especially so it seems when referring to research done using oral anabolics. Is the reason for this that they are ?more toxic ?than other oral preparations? Is it that they are taken more frequently? Or taken at higher dosages? Let?s look at that for a minute.

The Liver removes toxins from the blood. However we wish to look at it any oral medication is perceived to be a toxin by the research subject?s body- let?s use a rat for example. There are several ways to make a substance effective in spite of how efficient the liver is at removing the toxin from our research subject?s blood. One way is to simply dose the substance extremely high. So for example if an effective dose of acetaminophen (aka Tylenol) administered to rats would be 3mgs (purely hypothetical) the dosage could be as high as say 50mg. The liver would remove the majority of the acetaminophen, say all but the 3mg effective dose. While this is often demonstrated in over the counter preparations used in our research it is pretty inefficient and certainly not a cost effective way to overcome the livers extreme efficiency at removing toxins. Another way is to chemically alter the substance. This is what is most commonly exemplified in oral anabolics. It is referred to as methylation or 17 alpha akylation. It is the addition of a methyl group to the parent substance. The liver works to remove the methyl group, leaving the vast majority of the substance available and active in the research subjects system to do its job. It is an extremely effective delivery method and very effective at overcoming the livers efficiency at removing toxins. However it also causes the liver to work extremely hard, results in an elevation of liver enzymes, a decrease in the flow of bile, and has the potential to result in liver damage to various degrees.

This is where udca comes in. Now there are many herbal preparations out there than claim to do this and that for the liver in our research subjects, however, udca has solid science and documented research proving its efficacy at protecting as well as repairing the liver.

udca, or Ursodeoxycholic Acid, is proven to reduce elevated liver enzymes ? the marker used in research subjects to measure liver duress, strain or impairment. Much of the damage caused to research test subjects when administering oral anabolics is due to the impairment of bile flow. Many of the salts in bile are actually toxic and cause liver cells death. udca increases the rate of bile flow, reducing the back up of these toxic bile salts, thus greatly reducing the cell damage or even death they may cause. udca is also proven to reduce cholesterol absorption.

All the things that we read about these herbal liver cleansing preparations claiming to do that have absolutely no solid research backing them up; udca really does and does effectively. If used when administering an oral anabolic to research subjects, it minimizes the adverse impact. If used post administration it reverses the adverse impacts. All in all, udca is a must have for our research when administering oral anabolics to research subjects. It truly is a proven, essential supplement for our research arsenal.

Check it out >> Ursodeoxycholic Acid (UDCA)

Refs:
*Lindor KD, Kowdley KV, Luketic VA et al. (September 2009). "High-dose ursodeoxycholic acid for the treatment of primary sclerosing cholangitis". Hepatology 50 (3): 808?14. doi:10.1002/hep.23082. . PMC 2758780. PMID 19585548
*Kotb MA (July 2008). "Review of historical cohort: ursodeoxycholic acid in extrahepatic biliary atresia". Journal of Pediatric Surgery 43 (7): 1321?7. doi:10.1016/j.jpedsurg.2007.11.043. PMID 18639689
*Jackson H, Solaymani-Dodaran M, Card TR, Aithal GP, Logan R, West J (October 2007). "Influence of ursodeoxycholic acid on the mortality and malignancy associated with primary biliary cirrhosis: a population-based cohort study". Hepatology 46 (4): 1131?7. doi:10.1002/hep.2179
*Built to Survive: A Comprehensive Guide to the Medical Use of Anabolic ... - Michael Mooney, Nelson Vergel - Google Books





Seems to be good when using toxic orals.
I have not used it yet but will next time I use orals (probably spring)

you think usign it after oral use would be better than on cycle? I would think even starting it halfway in then a little bit passed when orals are stopped would be good?
 
CrazyTod said:
you think using it after oral use would be better than on cycle? I would think even starting it halfway in then a little bit passed when orals are stopped would be good?
Click to expand...

I'm absolutely no expert but did read a recommendation of 250mg ED while on a methylated compound. There was also a post that EOD might work just as well.
 
Muscle Gelz Transdermals
IronMag Labs Prohormones
Curt James said:

I'm absolutely no expert but did read a recommendation of 250mg ED while on a methylated compound. There was also a post that EOD might work just as well.
Click to expand...

I have heard this as well for a preventive dosing while talking a methylated compound. I heard for repair purposes the dose can be almost double this.
 
Where can udca, or Ursodeoxycholic Acid be purchased from?
 
CrazyTod said:
I was looking into this a while ago and found this posted on another forum:



Before we talk about this amazing substance, let?s talk about what prompts its necessity in our research at all. Hepatoxicity, or liver toxicity, is often associated with administration of oral preparations/medications. This is especially so it seems when referring to research done using oral anabolics. Is the reason for this that they are ?more toxic ?than other oral preparations? Is it that they are taken more frequently? Or taken at higher dosages? Let?s look at that for a minute.

The Liver removes toxins from the blood. However we wish to look at it any oral medication is perceived to be a toxin by the research subject?s body- let?s use a rat for example. There are several ways to make a substance effective in spite of how efficient the liver is at removing the toxin from our research subject?s blood. One way is to simply dose the substance extremely high. So for example if an effective dose of acetaminophen (aka Tylenol) administered to rats would be 3mgs (purely hypothetical) the dosage could be as high as say 50mg. The liver would remove the majority of the acetaminophen, say all but the 3mg effective dose. While this is often demonstrated in over the counter preparations used in our research it is pretty inefficient and certainly not a cost effective way to overcome the livers extreme efficiency at removing toxins. Another way is to chemically alter the substance. This is what is most commonly exemplified in oral anabolics. It is referred to as methylation or 17 alpha akylation. It is the addition of a methyl group to the parent substance. The liver works to remove the methyl group, leaving the vast majority of the substance available and active in the research subjects system to do its job. It is an extremely effective delivery method and very effective at overcoming the livers efficiency at removing toxins. However it also causes the liver to work extremely hard, results in an elevation of liver enzymes, a decrease in the flow of bile, and has the potential to result in liver damage to various degrees.

This is where udca comes in. Now there are many herbal preparations out there than claim to do this and that for the liver in our research subjects, however, udca has solid science and documented research proving its efficacy at protecting as well as repairing the liver.

udca, or Ursodeoxycholic Acid, is proven to reduce elevated liver enzymes ? the marker used in research subjects to measure liver duress, strain or impairment. Much of the damage caused to research test subjects when administering oral anabolics is due to the impairment of bile flow. Many of the salts in bile are actually toxic and cause liver cells death. udca increases the rate of bile flow, reducing the back up of these toxic bile salts, thus greatly reducing the cell damage or even death they may cause. udca is also proven to reduce cholesterol absorption.

All the things that we read about these herbal liver cleansing preparations claiming to do that have absolutely no solid research backing them up; udca really does and does effectively. If used when administering an oral anabolic to research subjects, it minimizes the adverse impact. If used post administration it reverses the adverse impacts. All in all, udca is a must have for our research when administering oral anabolics to research subjects. It truly is a proven, essential supplement for our research arsenal.

Check it out >> Ursodeoxycholic Acid (UDCA)

Refs:
*Lindor KD, Kowdley KV, Luketic VA et al. (September 2009). "High-dose ursodeoxycholic acid for the treatment of primary sclerosing cholangitis". Hepatology 50 (3): 808?14. doi:10.1002/hep.23082. . PMC 2758780. PMID 19585548
*Kotb MA (July 2008). "Review of historical cohort: ursodeoxycholic acid in extrahepatic biliary atresia". Journal of Pediatric Surgery 43 (7): 1321?7. doi:10.1016/j.jpedsurg.2007.11.043. PMID 18639689
*Jackson H, Solaymani-Dodaran M, Card TR, Aithal GP, Logan R, West J (October 2007). "Influence of ursodeoxycholic acid on the mortality and malignancy associated with primary biliary cirrhosis: a population-based cohort study". Hepatology 46 (4): 1131?7. doi:10.1002/hep.2179
*Built to Survive: A Comprehensive Guide to the Medical Use of Anabolic ... - Michael Mooney, Nelson Vergel - Google Books





Seems to be good when using toxic orals.
I have not used it yet but will next time I use orals (probably spring)

you think usign it after oral use would be better than on cycle? I would think even starting it halfway in then a little bit passed when orals are stopped would be good?
Click to expand...

Great post!
 
james-27 said:
Where can udca, or Ursodeoxycholic Acid be purchased from?
Click to expand...

I got a bottle from CEM 2 orders ago, for whenever my next oral run is.
I don't run orals often but that's no excuse NOT to have some sort of support/helper for the body.
I want my health to stay well so I avoid over using orals and use support supps when I do use them.
 
Mo_dash said:
Hey guys,I'm on Anavar,should i take TUDCA and when?
Thanks:)
Click to expand...

That is debatable to some. some may rec it the last couple weeks of oral use and continued for 2-4 more weeks after finished oral. but you could always just run it during, but I still do rec a couple extra weeks of udca after you have stopped the oral.

How are you using your anavar? whats your cycle?
 
Couple 1,000 mg of milk thistle just as effective??
 
I used to take milk thistle and liv 52 and so on. Now I stick with udca and nac when I run orals (which is less frequently than it used to be by the way).
 
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