tauroursodeoxycholic acid

[Betonarme]

Hi Everyone,

Has anyone ever used tudca? We've recently found information about this bile acid which supposedly can be used also to treat PBC (??) Below is study from a year 1996..

Looks like this acid is freely available throughout the Europe. I wonder which Brand is better.

Link:

ncbi.nlm.nih.gov/pmc/articl...

[Hidden]

Hello Betonarme.

Well looking online, there is nothing on our UK reputable sites I could find about this TUDCA. Seems it is something as a supplement that reading between the lines for body builders. I think it is taurine that we produce naturally.

Personally, I don't think I'd want to risk taking. Plus you never know what you are buying unless from a reputable company and then there can be problems with that....

....I know in the UK now there has been new legislation regarding health supplements. Milk thistle that some take for liver health is one that has now to be licensed.

I think if this was TUDCA was in use in PBC I do think that it would be known about?

[Betonarme in reply to Hidden]

Yes, I had the same concerns like you and wanted to ask the forum first.....I searched the phrase in the "Healthunlocked Web" but no mention of it in the past, at least not in the PBC foundation but one single discussion in the " AMN EASIER" forum.

Anyway....this is indeed strange...academic papers tells about it's similar (even better) effects like UDCA and it's a different substance (molecule) than UDCA. It's more hydrophilic. Some people get unresponsive to UDCA over the time and I thought TUDCA can still work for them may be.

Turning the course of the discussion, my wife seems to becoming slowly unresponsive to UDCA and yet she does not want to start with OCA because of possible serious side effects and it's relatively new without long term safety. With serious side effects i don't mean severe Itch but as I wrote in one of my earlier posts, OCA activates FXR receptors which in turn activates FGF-19 (member of FGF family) and there are many papers indicating that over expression of FGF19 (ligand for FGFR-4 receptor) is involved and correlates with hepatocellular carcinoma and poor prognosis. The risk is to cure PBC one can cause much worse condition. What I couldn't understand still is that whether FGF-19 is a cause (or promoter) or consequence of HCC.

I guess ours is not merely a paranoia since there is already one biopharma company working on a lab engineered version of FGF-19 to eliminate possible danger and there are countless other studies and papers about the relationship between FGF19 and progression of Liver Tumor (HCC)

Link: ngmbio.com/pipeline/ngm282/

Below is some further information:

Talking about over-expression:

>>

Obeticholic acid (OCA, alsoknown as 6 a-ethyl-CDCA and INT–747) is about

100-fold more potent an FXR agonist than CDCA. Clinical trials of OCA in primary biliary cirrhosis (PBC) and nonalcoholic steatohepatitis (NASH) have been published or are in progress, with treated patients showing apparent dose-dependent increases in FGF19.

onlinelibrary.wiley.com/doi...

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Talking about FGF19 and HCC:

>>

Targeted inhibition of the FGF19-FGFR4 pathway in hepatocellular carcinoma; translational safety considerations."

Abstract

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death and new therapies are urgently required to treat this disease. Recent data suggest that the FGF19-FGFR4 axis may be a key driver in certain forms of HCC, making the pathway an interesting, emerging molecular target for potential therapeutic intervention. A complication is that, outside of malignant disease, FGFR4 plays an important physiological role in the regulation of hepatic bile acid (BA) synthesis. FGF19 signalling via FGFR4 suppresses de novo BA production in the liver, tightly maintaining hepatic and systemic levels of these detergent-like molecules at a physiological threshold and preventing pathological complications of raised BA levels, such as cholestatic liver injury and bile acid diarrhoea. In some cases of HCC, the malignant disease causes bile duct obstruction, preventing BA secretion from the liver and resulting in cholestasis. Here, the role of FGFR4 signalling in both HCC and BA homoeostasis is discussed. The potential effects of therapeutic FGF19-FGFR4 inhibition on human hepatobiliary/gastrointestinal physiology are considered along with the potential safety implications of FGF19-FGFR4 blockade in patients with HCC.

ncbi.nlm.nih.gov/pubmed/243...

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And a Kind of UDCA and TUDCA comparison:

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Results

: Serum liver enzymes related to cholestasis and cytolysis consistently improved, as compared to baseline values, during the administration of both ursodeoxycholic and tauro-ursodeoxycholic acids, but no signiÆcant difference between these two bile acids was found. Both treatments were well tolerated and no patient complained of side effects.

Conclusion

: In the short-term, tauro-ursodeoxycholic acid appears to be safe and at least as effective as ursodeoxycholic acid for the treatment of primary biliary cirrhosis.

onlinelibrary.wiley.com/doi...

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Sorry for the long message

[mrspeffer2]

Good Morning....I tried it in the past, but not correctly. I cannot tolerate Urso, so have searched for alternatives. My belief is that the fillers in Urso is what causes the intolerance for me.I recently have been re diagnosed after 20 years. First they said, no PBC, but medication induced liver injury. Now I'm being told I am truly AMA neg PBC plus liver injury. My elastography shows minimal scaring, bilirubin is perfect. My LFT's are always high.

Of course, the doctor wants to put me on URSO. I refuse. I am going back on TUDCA.

I am including an article regarding it. These folks recommend a TUDCA by Double woods,500mg formula. VERY clean.

Sorry, I could not get the link, but here is what I found:

Tauroursodeoxycholic acid for treatment of primary biliary cirrhosis. A dose-response study

A Crosignani 1 , P M Battezzati, K D Setchell, P Invernizzi, G Covini, M Zuin, M Podda

Affiliations expand

PMID: 8674405 DOI: 10.1007/BF02213140

Abstract

Tauroursodeoxycholic acid, a highly hydrophilic bile acid, may be of therapeutic value for chronic cholestatic liver diseases. We performed a dose-response study on 24 patients with primary biliary cirrhosis who were randomly assigned to receive 500, 1000, or 1500 mg daily of tauroursodeoxycholic acid for six months. Biliary enrichment with ursodeoxycholic acid ranged from 15% to 48% and was not related with the dose. Serum liver enzyme levels decreased significantly after the first month of treatment with all the three doses. No significant difference among the three doses was found, although further reduction over time occurred with 1000 and 1500mg daily. Plasma total and HDL cholesterol significantly decreased in patients administered the two higher doses. Diarrhea was the only side effect. In conclusion, a dose of about 10mg/kg body wt/day of tauroursodeoxycholic acid should be used for long-term studies in patients with primary biliary cirrhosis.