Coffee and fibrotic progression

[yodennis]

I see quite a few of you recommend 3 cups of coffee daily relative to fibrosis (I have C, a history of failed treatments, and cirrhosis) and I have read the advocating articles. I find the taste of coffee terrible. Are their any alternative means of digestion. Last I read the fibrosis-prophylaxis-responsible-agents within coffee were still ambiguous. Have anyone isolated the ingredient within coffee responsible. I have to add I'm quite "addictive" and have never had 3 of anything and stopped if I liked it so defeating my aversion to coffee might lead me to a support group. My best. d

[yodennis]

I meant to request alternative means of "ingestion"!

[Trinity4]

Cocopure, it's the bomb.  Full of antioxidants and tastes wonderful.  I have no affiliation with the company, I receive no kickbacks nor do I promote it's usage through subliminal advertising and I do not operate under the guise it is guaranteed to reduce fibrosis so that I may monetarily gain from it.   All I know is it is delightful to the palate and is good for you.  

Trinity

[Trinity4]

Having given the disclaimer above here is the website which I acutally forget to include in my post.

http://www.cocopuretea.com/

[portann]

I'm not a coffee lover, either, but if I let my husband fix it up, I'm always able to drink it.

That's because he has zero inhibitions about loading it up with cream and sugar (yeah, not good for you) and wow, it goes down so easy.

Coffee does seem to get a lot of good press. This is from 2010 and as you can see, low dose maintenance interferon is off the table as an anti-fibrotic but coffee is hot. Note that it's not likely the caffeine, as tea is ineffective:

Complementary Medical Strategies
Among the general population, interest in complementary or alternative medicine (CAM) is significant. Although convincing data for efficacy are lacking, CAM approaches are widely used and are generally thought to be safe. One of the interesting findings from the HALT-C study was that regular coffee intake (>3 cups/d) [48] was associated with lower rates of disease progression in CHC patients [47]. The active ingredient remains unclear; it is unlikely to be caffeine, because tea intake was not beneficial. Other potential antifibrotics include milk thistle (active compound = silymarin [silybinin-1/2]), TJ-9 (baicalein), TJ-135 (emodin), coptis (berberine), turmeric (curcumin), and red wine (trans-reservatrol). Many of these agents are believed to have antioxidant properties that may reduce inflammation.

http://www.springerlink.com/content/25g827154j696057/fulltext.html

[WillinSD]

Identification of paraxanthine as the most potent caffeine-derived inhibitor of connective tissue growth factor expression in liver parenchymal cells.
Gressner OA, Lahme B, Siluschek M, Gressner AM.
Source
Institute of Clinical Chemistry and Pathobiochemistry, Central Laboratory, RWTH-University Hospital, Aachen, Germany. ***@****
Abstract
BACKGROUND:
Recently, we identified hepatocytes as the major cellular source of profibrogenic connective tissue growth factor (CTGF/CCN2) in the liver. Based on reports of a hepatoprotective effect of coffee consumption, we were the first to provide evidence that caffeine suppresses transforming growth factor (TGF)-beta dependent and -independent CTGF expression in hepatocytes in vitro and in vivo, thus suggesting this xanthine-alkaloid as a potential therapeutic agent.

AIM:
This study aims at comparing the inhibitory capacities of caffeine and its three demethylated derivates paraxanthine, theophylline and theobromine on CTGF expression in hepatocytes and hepatic stellate cells (HSC).

RESULTS:
Our data suggest paraxanthine as the most important pharmacological repressor of hepatocellular CTGF expression among the caffeine-derived metabolic methylxanthines with an inhibitory dosage (ID)50 of 1.15 mM, i.e. 3.84-fold lower than what is observed for caffeine. In addition, paraxanthine displayed the least cell toxicity as proven by the water-soluble tetrazolium-1 cell vitality assay. However, caffeine or any of the metabolites did not inhibit CTGF expression in HSC. At the toxicological threshold concentration of 1 mM for paraxanthine, we observed an inhibition of hepatocellular CTGF synthesis by 44%, which was strongly reverted in the presence of the specific competitive cyclic adenosine monophosphate inhibitor Rp-adenosine 3',5-cyclic monophosphorothioate triethylammonium salt. Furthermore, CTGF protein expression induced by various concentrations of TGF-beta (0.13-1 ng/ml) is still reduced by, on average, 27%/45% in the presence of paraxanthine (1.25 mM/2.5 mM).

CONCLUSION:
Our data provide an evidence-based suggestion of the caffeine-derived primary metabolite paraxanthine as a potentially powerful antifibrotic drug by its inhibitory effect on (hepatocellular) CTGF synthesis.

PMID: 19291178 [PubMed - indexed for MEDLINE]