The ultimate LIVER thread and info on orals and ORAL TOXICITY!!

[Atomini]

This post might deserve a sticky, seeing as though there is no definitive post around here concerning liver health and oral C17 alpha alkylated anabolics. No post stating what specifically happens inside the liver when C7AA steroids are consumed, what they do inside, what happens over prolonged periods, and what is the best thing to do and take in order to solve the problem. The answers to all of these questions have recently piqued my interest because in one of my biochemistry courses, we just so happen to be covering certain aspects of liver function and the biochemical processes that occur inside it. We specifically touched upon the use of ursodeoxycholic acid (UDCA) for regulating proper liver function (specifically, BILE FLOW) in the midst of liver damage from things like alcohol, hepatitis C, etc. I also ran into a small issue post-cycle that I thought may have been a liver issue (lucky it doesn't seem like it was), and that caused me to look further into this. Some or much of this information may already be known, but I feel the need to spread word about it and post this here to educate people who might be asking the same questions.

I'm a really busy guy, and I don't have very much time to take everything I have read and conjure it up into my own words here. So, to save time, I am simply going to copy and paste my findings from other sources into this post, and provide references to them.

I am, for the most part, going to just copy and paste a whole post I already made in a previous thread I posted in where a forum member was asking about liver protection, oral anabolics, etc. where I explained everything to him. Here it is, folks:

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I want to start off by saying this: milk thistle is garbage. TUDCA (Tauroursodeoxycholic acid) is quite literally the primary and ONLY liver protectant people should be using if they are taking C17 Alpha Alkylated oral anabolic steroids. I think that Liv 52 is okay to use as well. But, if you could only pick ONE product and throw the rest away, I would say TAKE THE TUDCA!!!! Research has shown that it is the ONLY thing that is effective at treating anabolic steroid SPECIFIC induced cholestasis of the liver. Off the top of my head, one company that makes a product with TUDCA in it is Thermolife in their Liver Longer supplement, but they have seemed to be out of stock for a long while now. I know it is possible to pick up generic TUDCA if you look hard enough online. Just google it!

If you can find TUDCA elsewhere, get it as soon as you can.

As a matter of fact, using a liver support supplement such as TUDCA may even INCREASE the oral absorption and bioavailability of the steroid because it prevents cholestasis of the liver. You have to understand what happens in the liver when you use C17 alkylated orals. Cholestasis is defined as an impairment of bile flow in the liver. I don't know if you remember your highschool biology class, but bile is an extremely important component of the liver and of our body, because bile serves dual purposes:

1. In a way, it acts as a waste removal sewage fluid for the liver. All of the byproducts (not all necessarily bad, but stuff that your liver needs to remove on a regular basis or else it will harm the liver from an unhealthy buildup) that your liver creates from all the work it does in metabolizing a bazillion billion different things every day, gets collected as bile. In turn, bile salts really 'clean' the liver out.

2. Bile and the bile salts within it are very important to our digestion, especially of fats. It's stored in the gall bladder and then pumped into your duodenum (upper section of your small intestine) when you eat food to aid in digestion, as it assists in the breakdown of fats and such.

Now, in a nutshell, what happens when your liver gets 'damaged' from oral steroids is: (and i'm not going to get into the specific chemistry of it for ease of explanation to the layman) the liver is overloaded from processing the C17 alkylation on the anabolic steroid you are ingesting. What happens as a result is that it causes a slow down of bile flow in the liver, because the liver is getting so overloaded with the processes it is trying to undergo. The impairment of bile flow in the liver is known as cholestasis, and is a direct result of C17 alkylated steroid use . When bile flow is slowed down too much (or has outright STOPPED), the bile salts, which are very toxic to the liver cells, will start to damage those liver cells. The key idea here is BILE FLOW, and you'll see this repeated a lot in this post! The liver needs to keep churning bile through itself in all of its cells in order to clean out the metabolites resulting from all of the biochemical processes it's doing every second!

I don't have much time on me, so for further explanation I am going to quote a couple articles I found that explain in more detail what TUDCA does and how it literally is the ONLY liver support compound that is useful, to a much larger degree than anything else, at combating cholestasis:

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.

Another article:

How do 17-aa oral steroids cause liver damage?

Despite a lot of discussion on the forums about the "toxicity" of different oral steroids, most users are unaware of the mechanism or implications around these "toxic effects" (which is probably the reason why most users have yet to find an effective cure for the toxic effects).

Let me shed some light on this ambiguous topic.

17-aa steroids are toxic to the liver because they inhibit the excretory functions of the liver. (1-7)

More specifically, the more "liver toxic" a 17-aa steroid is, the more it inhibits the production and flow of bile from the liver.

Bile salts are known as the liver's "cleansing agents" because they act as "soaps" that carry away the toxins and flush them into the intestines for excretion. If the bile flow is restricted in the liver, then the liver cannot rid itself of toxins. When the liver loses its ability to excrete toxins, it creates a buildup of toxins throughout the entire body. (1-13)

This condition is known as cholestasis [Kola-sta-sis]. By definition, cholestasis is a condition where the flow of bile cannot flow from the liver. (1) This is the most common liver condition developed from 17-aa steroids. (1-7)

If a liver becomes cholestatic for too long, the condition can begin damaging liver cells by causing necrosis (premature death of liver cells) from excessive toxin build up in the liver. This can eventually lead to cirrhosis of the liver (development of fibrous scar tissue) when the liver attempts to regenerate the damaged liver cells. This leads to loss of liver function from the replacement of healthy liver cells with fibrous connective tissue. (2)

Although cholestasis is reversible and generally not a lethal condition, it can lead to the more serious problems mentioned above if left untreated -- not to mention costly medical bills.

To avoid serious health complications it's important to protect the liver before it becomes cholestatic or seriously damaged from prolonged cholestasis (which I will explain later).



What are signs that my liver is damaged?

When the liver has been damaged by oral steroids there are certain signs that may become obvious to the user.

Here are some of the most common signs indicating you may have a serious liver issue. Warning signs usually appear in the following order, with the later signs being the most serious -

• Reduced appetite
• Nausea and fever
• Excessive Itchiness
• Yellow eyes or skin (jaundice)
• Very dark urine (dark amber colored)
• Bloody stools


Waiting for all these signs to appear means you have waited too long. You want to take action BEFORE these signs appear. This is why I advise getting full lab values on liver function before, during and after any 17-aa oral steroid cycle. If performing lab tests for liver function, the following values are considered normal.


Normal Values -

Total bilirubin range: 0.3-1.7 mg/dl

Alanine aminotransferase (ALT) range: 10-40 IU/L

Aspartate aminotransferase (AST) range: 10-40 IU/L

Alkaline phosphatase (ALP) range: 34-125 IU/L

Gamma-glutamyl-transpeptidase (GGT) range: 7-32 IU/L

Levels above these normal values doesn't necessarily mean you have liver damage. It is common for healthy weight training athletes or bodybuilders to be slightly outside of the "normal" ALT, AST and ALP values. Therefore these "Danger Values" have been established as more appropriate levels to indicate a serious liver toxicity issue. (1-7)


Danger Values -

Total bilirubin: 10 mg/dl or higher

Alanine aminotransferase (ALT): 50 IU/L or higher

Aspartate aminotransferase (AST): 50 IU/L or higher

Alkaline phosphatase (ALP): 150 IU/L or higher

Gamma-glutamyl-transpeptidase (GGT) range: 50 IU/L or higher
NOTE: Historical research from 17-aa oral steroid induced liver toxicity suggests that lab values higher than the "Danger Values" indicate that you may be suffering from cholestasis (1-7) If your lab values are higher than the "Danger Values" listed above you should discontinue any current oral steroid use and seek medical treatment.

If the above lab tests are not an option, it is possible to get an affordable at home test for bilirubin levels, which can help diagnose a liver damage from a 17-aa oral steroid. There are tests available, such as the TestMedica Liver Home Scan, which can be purchased online for less than $5 per test. Although these home based tests lack accuracy or true diagnosis ability, it can offer a valuable insight about the condition of the liver and is recommended for any steroid user not able to get lab tests done in a clinical setting.



How can I protect my liver?

To prevent cholestasis, the primary condition caused by oral steroid use, it is important to ensure there is ample hydrophilic bile acid available in the liver for the proper clearance of toxins. There are two reliable options for this.

1. The first option is the drug known as Ursodiol - a.k.a. ursodeoxycholic acid. This naturally occurring bile acid is used for its ability to detoxify the liver by clearing out less hydrophilic bile acids and other toxins that cause a toxic build up, such as 17-aa oral steroids. (4,5)

Ursodiol is typically prescribed to patients admitted to the hospital for steroid induced liver toxicity, but unfortunately, it is an expensive prescription drug, and not easily obtainable.

Typical dose - 1000-1200mg/day before, during and after cycle

One more small thing I found someone post on another forum:

Everytime now that I take an oral AAS, I get massive heartburn within 3 days. I even tried an injectable oral and still got acid reflux within a week. So, I did some research and found some interesting information. This is just a random post I found on Google.


http://www.********.com/forums/archi...p/t-36636.html
Everyone seems to miss what is happening here. If an oral kills your appetite, it is because it is too toxic for the liver. I forget exactly what happens, but to summarize, when the liver is overloaded it causes a slowing of digestion, and a backflow of bile, which is why you also see people complaining of acid reflux on harsh 17aa's. The only way to really cure your appetite is to drop the anadrol . Perhaps next time around run with liv. 52 and alpha lipoic acid?



From what I read, bile helps with digestion. Now, when I take an oral AAS, the pain I get is similar to acid reflu/heartburn, but not exactly. It feels more like the food I eat just sits in my stomach and rots, never digesting. Lets say I eat some tacos on Tuesday, by Thursday morning I am still burping that taste up.That always made me wonder if orals cause heartburn or something similar.




Now read this
http://www.emoryhealthcare.org/liver...blems.html#PBC

In primary biliary cirrhosis, inflammation destroys the bile ducts and prevents bile from escaping the liver. The accumulated bile damages healthy liver tissue, eventually leading to cirrhosis (scarring). As scar tissue replaces healthy liver tissue, the liver loses its ability to function. All this happens very slowly. People with PBC can lead healthy, symptom-free lives for 10 years or more after diagnosis.

Though primary biliary cirrhosis is often asymptomatic, especially early on, the most common symptom is extreme itching, especially in the arms, legs and back. Other symptoms include fluid buildup in the abdomen or legs, jaundice (yellowing of the eyes and skin), or fatty deposits and darkening of the skin under the eyes.

The standard treatment for PBC is a daily dose of a medication called ursodiol. Ursodiol improves liver function and increases life expectancy in people with PBC. Other medications may be indicated for controlling symptoms

I hope this has educated a lot of people! Keep this thread bumped!

[Chris_Sweden]

Great post!
Was just about to order some Liv 52, but now I'll definitly make it TUDCA instead.
What is the recomended daily dosage for tudca?
I found it for $25/60 caps. Is that ok or should I keep looking?

[Atomini]

- 500mg PER DAY for liver maintenance while on cycle.

- 1,000mg or more per day for liver repair if you have done lots of damage from heavy oral use and/or you have high liver enzyme readings from a blood test, etc.

The medical studies done on UDCA/TUDCA on people with liver disorders were using 1,500 - 2,000mg per day for repair purposes.

[MickeyKnox]

Excellent write up, as usual, Atomini!

Any experience with Aegis‏? (Polyenylphosphatidylcholine + Tauroursodeoxycholic acid)

http://www.antaeuslabs.com/aegis.html

[Chris_Sweden]

- 500mg PER DAY for liver maintenance while on cycle.

- 1,000mg or more per day for liver repair if you have done lots of damage from heavy oral use and/or you have high liver enzyme readings from a blood test, etc.

The medical studies done on UDCA/TUDCA on people with liver disorders were using 1,500 - 2,000mg per day for repair purposes.

Thanks, great info!
I will start a 12 week Test-C cycle soon, with orals such as Dianabol (30 mg ed) and Proviron (25 mg ed) the first 6 weeks. Will 500-1000 mg of TUDCA ed make it possible for the liver to manage the orals throughout the 12 week cycle? I just LOVE that D-bol! But I've had some issues with water retention though. Hopefully some Proviron and Aromasin will help.

[Atomini]

Excellent write up, as usual, Atomini!

Any experience with Aegis‏? (Polyenylphosphatidylcholine + Tauroursodeoxycholic acid)

http://www.antaeuslabs.com/aegis.html

No experience with them but I will be using their stuff very soon. I have heard very good things about it though.

Thanks, great info!
I will start a 12 week Test-C cycle soon, with orals such as Dianabol (30 mg ed) and Proviron (25 mg ed) the first 6 weeks. Will 500-1000 mg of TUDCA ed make it possible for the liver to manage the orals throughout the 12 week cycle? I just LOVE that D-bol! But I've had some issues with water retention though. Hopefully some Proviron and Aromasin will help.

I wouldn't run oral AAS for more than 6 weeks at a time, especially the stuff that can be a little harsher at times such as dbol or anadrol . The TUDCA/UDCA may allow you to run it longer, yes, but I like to err on the side of caution. I don't see a problem with doing this, but it's not something I would do.

[MickeyKnox]

No experience with them but I will be using their stuff very soon. I have heard very good things about it though...

Thanks Atomini, have some in the mail.

Btw, why is this not a sticky???

[JohnnyTribal]

This is an amazing price if info I love this board

[Chris_Sweden]

I'll go for 6 weeks. Better safe than sorry, right?
Thanks again, Atomini, this thread has been very helpfull!

[Schyluer]

Atomini i have gilberts syndrome/disease. This was a great write up i learned a lot. Was wondering if this still applys to me and to those who have gilberts syndrome. Thanks buddy

[kawika]

Can this be a sticky yet? such good info

[Atomini]

Hey guys, sorry for the late response, I never check this forum and I just noticed out the corner of my eye that this thread had some new replies in it.

Chis sweden, 6 weeks of TUDCA/UDCA is good, you just don't want to go over 8 weeks without a break.

Schyluer, I don't know anything about gilberts syndrome, but if you do some extensive searching and research on TUDCA/UDCA, you should find all the information you need. I hope i've provided enough thus far for you.

[kawika]

Atomini. I just got my bw back and apparently my liver enzymes are elevated far above normal (I haven't seen the results myself, they are in the mail). I haven't done an oral cycle in almost a whole year and i have no idea whats causing the elevated enzymes; in fact bw last aug showed normal liver function. But my question is could udca help liver even though no oral aas have been used? Also is clen liver toxic? I recently started some clen and want to make sure im not doing more damage to my liver

[Atomini]

Atomini. I just got my bw back and apparently my liver enzymes are elevated far above normal (I haven't seen the results myself, they are in the mail). I haven't done an oral cycle in almost a whole year and i have no idea whats causing the elevated enzymes; in fact bw last aug showed normal liver function. But my question is could udca help liver even though no oral aas have been used? Also is clen liver toxic? I recently started some clen and want to make sure im not doing more damage to my liver

Yes, it would help. But it depends on what your elevated liver enzymes are the result of. It wouldn't hurt to try taking TUDCA/UDCA regardless.

Clenbuterol 's liver toxicity is inconsistent. It has been shown to be slightly, yet other observations have not shown it to be liver toxic at all. No conclusions there unfortunately. For safety, if I were you, I would drop the clen whether or not it is the cause.

[kawika]

Yes, it would help. But it depends on what your elevated liver enzymes are the result of. It wouldn't hurt to try taking TUDCA/UDCA regardless.

Clenbuterol's liver toxicity is inconsistent. It has been shown to be slightly, yet other observations have not shown it to be liver toxic at all. No conclusions there unfortunately. For safety, if I were you, I would drop the clen whether or not it is the cause.

Thanks for the advice. My next goal is to find out what's causing this liver damage. I really appreciate you sharing your knowledge and expertise on the matter.

[Liftheavy6]

I'm reading a lot of your posts, I'm learning a lot. Thanks bro

[Armykid93]

Hey atomini i'm curious.

How long should the break between tudca usage be? You say 8 Weeks is the longest to run it but after running it that long how long should one be off before starting it again.

When should one start using it in conjunction to a regular cycle of only injectable aas and when with orals being added in? I'm guessing the times you need to start are going to be different depending.

Also is tudca something you would want to use if your not on cycle as a form of liver health or is it to strong for that? I'm assuming it is.

[tigerspawn]

Thanks for keeping this thread alive

[CanadianBeefcake]

Bump! Great thread. Thanks for the info Atomini

[Isochroma]

Curcumin beats UDCA (and likely TDCA) and everything else for liver protection and regenation save high-CB2-agonist synthetic cannabinoids. Not to mention Curcumin is far cheaper than TDCA:

EFFECTS OF CURCUMIN, RESVERATROL AND URSODEOXYCHOLIC ACID ON ETHINYLESTRADIOL AND CHLORPROMAZINE-INDUCED INTRAHEPATIC CHOLESTASIS IN RATS.pdf

pharmacologyonline.silae.it/files/archives/2009/vol3/010.Dina.pdf

Check that PDF's graphs starting on PDF page 5/10.
You'll be shocked by the liver histopathology images on PDF page 6/10.

"Concurrent CMN administration with EE-CPZ
prevented the proliferation of bile ducts. Liver sections showed normal liver structure with normal
bile ducts (figure 3A). RSV administration did not prevent the proliferation of bile ducts (figure
3B). UDCA produced a decrease in the degree of proliferation of bile ducts compared to untreated
control group (figure 3C)."

[bosley1]

Curcumin beats UDCA (and likely TDCA) and everything else for liver protection and regenation save high-CB2-agonist synthetic cannabinoids. Not to mention Curcumin is far cheaper than TDCA:

EFFECTS OF CURCUMIN, RESVERATROL AND URSODEOXYCHOLIC ACID ON ETHINYLESTRADIOL AND CHLORPROMAZINE-INDUCED INTRAHEPATIC CHOLESTASIS IN RATS.pdf

pharmacologyonline.silae.it/files/archives/2009/vol3/010.Dina.pdf

Check that PDF's graphs starting on PDF page 5/10.
You'll be shocked by the liver histopathology images on PDF page 6/10.

"Concurrent CMN administration with EE-CPZ
prevented the proliferation of bile ducts. Liver sections showed normal liver structure with normal
bile ducts (figure 3A). RSV administration did not prevent the proliferation of bile ducts (figure
3B). UDCA produced a decrease in the degree of proliferation of bile ducts compared to untreated
control group (figure 3C)."

A couple of things with this: the dosage of curcumin was 200mg/kg. The dosage of udca was 25mg/kg. Udca was also administered simultaneously with ee-cpz. I believe there have been other studies (no refs soz) showing it to be more beneficial as an after the fact treatment, and in fact harmful as a before the liver insult preventative. The study was only 7 days. Used over time udca has a cumulative affect. Is 7 days enough? Curcumin is healthy though. Nothing against that. Lets not disregard udca too quickly though.

[SOL!D5NAK3]

i can't find any TUDCA in our country drug info site but i did find UDCA, they have 300mg and 250mg forms.

is UDCA alone enough for liver protection?

[Gambit11]

Trying to order some online. Overwhelmed with amount of brands, Variation of prices, and insufficient info on content dose. Can someone recommend a brand.. please.

[minto]

Trying to order some online. Overwhelmed with amount of brands, Variation of prices, and insufficient info on content dose. Can someone recommend a brand.. please.

Been getting mine on tudca.com recently, no complaints so far.

[Mr.BB]

i can't find any TUDCA in our country drug info site but i did find UDCA, they have 300mg and 250mg forms.

is UDCA alone enough for liver protection?

Same here, I can only find Ursofalk (UDCA) in pharmacies. Its a prescription only medicine. Going to try it.

[mrtypr]

Hey guys

I am just trying to work out how much TUDCA I should have as I finished a cycle over 10 weeks and my liver enzymes are a little elevated:

Boldenone Undecylenate @ 450mg
Testosterone Enanthate @ 450mg
Trenbolone Enanthate @ 300mg

through week 5 to 10 I did 50mg on var

followed by a month of Clomid and Nolva standard protocol


my liver enzyme are as follows:
AST is 45 and ASL is 116
Imgur: The most awesome images on the Internet

I wrote 45 myself as the doc did not include it in the report as it was healthy

Now I know the post says from the OP reply:

500mg PER DAY for liver maintenance while on cycle.

- 1,000mg or more per day for liver repair if you have done lots of damage from heavy oral use and/or you have high liver enzyme readings from a blood test, etc.

The medical studies done on UDCA/TUDCA on people with liver disorders were using 1,500 - 2,000mg per day for repair purposes.

Not sure if i need 1g of TUDCA per day as it seems a lot for my liver levels

also the dosage of whats suggested is that purely just Tauroursodeoxycholic acid ? as the TUDCA i am looking at has other stuff in there to such as;
PPC
NAC
SAMe

[Doublewide1]

I actually have liver problems. Old thread I know but this subject is near and dear to my heart. Is eveytone sold on the fact that Milk Thistle is crap? I live in U.S. but someone (a doctor) told me Milk Thistle is a prescription in other countries and the only reason you can buy it OTC here is because no one got a drug patent on it quick enough. Never heard of this other stuff but will read it.

As for steroids it’s all what you taking. Orals are particularly harsh on the liver. And of course you can read up on which injectibles are the most liver toxic. Some just kill your liver. I have done a lot of research on this and the safest steroids to take are Test Prop and NPP. From my research there I’d very little if not zero effect on your liver. This is all I can take.

How bad were my liver problems? One of my liver levels sai “Panic High”. Not Low. Not high. Panic High. Never heard of that before. I was having some pretty big problems. Well, nou pretty big. They were huge problems.

[Donthate]

That is a lot of useful information, thank you