Thursday, January 27, 2011

Natural supplements to improve liver fibrosis; Curcumin/Turmeric/Curry, Blueberries, Milk Thistle, and Coffee.

Is there a natural way to improve liver fibrosis ?
In this entry the goal is to explore published data on natural alternatives to fight or curtail liver damage.
Obviously this blog is about Hepatitis C, with that said, this needs to be said; there is no verified/published data or information that has established a natural cure for HCV. It just ain't so folks.
Fatty Liver Disease
Liver damage and fibrosis associated with fatty liver disease has become a major health concern. According to the American Liver Foundation up to 25% of adults with NASH may have cirrhosis. The good news is there are healthy strategies to help reduce the amount of fat in the liver. A few things to consider are diet, exercise, and maintaining a healthy weight. Committing to this lifestyle can help reduce and possibly eliminate steatosis. A recent study found that HCV patients who participated in a diet and exercise program for three months lowered their grade of steatosis and, remarkably, their fibrosis score.
The relationship between fatty liver disease and HCV
Hepatitis C And Fatty Liver Disease; Non-alcoholic steatohepatitis or (NASH).

There are two different forms of steatosis (Fatty Liver) that may be found in people with HCV: Metabolic steatosis and HCV-induced Hepatic steatosis. .

Metabolic steatosis
Metabolic steatosis can coexist with HCV, regardless of genotype, in patients with risk factors such as obesity, hyperlipidemia, and insulin resistance. .

Hepatic steatosis
The second form of hepatic steatosis in HCV patients is a result of the direct cytopathic effect of genotype 3 viral infections. There have been proposed mechanisms for this process but it remains elusive. Both categories of steatosis tend to hasten the progression of liver fibrosis and therefore prompt recognition and management should be initiated in patients with HCV and steatosis.

Fatty liver disease in HCV has been proven to be caused directly from the virus. Genotype 3 patients are known to have a higher rate of fatty liver then other genotypes. Previously both genotype 2 and 3 were treated with the same treatment duration with the assumption both were the easier genotype to treat. Currently the data has shown that genotype 3 patients have a higher incidence of fatty liver and possibly the two genotypes may require different treatment protocols.

As a special note ; The new drug telaprevir ALONE or without adding SOC in an early study was potent against HCV Genotype 2 but not 3 ; The Best Results were seen when telaprevir was combined with Interferon/ribavirin.

Summary of the results;
Genotype 3 patients, SVR rates were lower overall : G3 telaprevir alone: SVR 50%; G3 telaprevir/pegylated interferon/ribavirin: SVR 67%; G3 pegylated interferon/ribavirin: SVR 44%.

Hepatitis C is not the only liver disease that causes liver damage, Non-alcoholic steatohepatitis or (NASH) recently has been reported as one of the leading causes of cirrhosis in adults in the United States. This month published in the Harvard newsletter were these statistics on fatty liver; 70% to 90% of people with obesity or diabetes develop fatty liver.
However if alcoholism is the cause, the fat from the liver can disappear, usually within 6 weeks, when people stop drinking. If the cause is not identified and remedied, fatty liver can have serious consequences. For example, if excessive alcohol use continues or a drug causing fatty liver is not stopped, repeated liver injury may eventually lead to cirrhosis. Treatment focuses on minimizing or eliminating the cause of fatty liver. People should stop taking a drug, lose weight, or take measures to control diabetes, lower triglyceride levels, or stop drinking.
Natural supplements to improve liver fibrosis

Curcumin/turmeric/curry, blueberries, Milk Thistle, and coffee.
The Data
Indian Spice Curcumin May Prevent Liver Damage
MedPage Today

March 24, 2010
Action Points
* Explain to interested patients that this study shows that curcumin appears to delay liver damage in mice. It has not been evaluated for this purpose in humans.
* Note that investigators believe curcumin might be pursued as a treatment for chronic cholangiopathies in humans.
A major component of the Indian spice turmeric was found to decrease inflammation and fibrosis in vitro and in an animal model of chronic cholangiopathy, a new study found.

Mdr2-/- mice fed curcumin, the compound that gives turmeric its bright yellow color, had reduced liver damage, cholestasis, and fibrosis compared with mice fed a normal diet (P<0.05>

"We demonstrate that curcumin is beneficial in a genetic mouse model of cholangiopathy and biliary fibrosis, and propose potential molecular and cellular targets of curcumin in this model," Michael Trauner, MD, of Medical University Graz in Austria, and colleagues wrote. "Collectively, our findings have important implications for understanding the pathophysiology of cholangiopathies and suggest that combined targeting of cholangiocyte and portal myofibroblasts activation could represent a central strategy to treat or delay the progression of chronic cholangiopathies and liver fibrosis."

Progressive inflammatory conditions of the liver include primary sclerosing cholangitis and primary biliary cirrhosis, which are characterized by inflammation, scarring, and destruction of the bile ducts inside and outside of the liver. Chronic cholangiopathies, which are usually genetic or autoimmune in origin, cause inflammation and fibrosis and can lead to the need for liver transplantation. Previous research in rodents with chemically induced liver damage and fibrosis found that curcumin has anti-inflammatory, antioxidative, and antifibrotic properties, the investigators noted. The compound comes from the rhizomes of the perennial herb Curcuma longa and has been used for centuries in Ayurvedic medicine to treat a wide range of gastrointestinal disorders.

But recent research suggests the chemical might have other medical applications, including possible effects on plaque in Alzheimer's disease. In the current liver study, investigators noted, it was unknown if curcumin could prevent bile duct inflammation and liver damage due to cholangiopathies. "Since the effectiveness of currently available medical therapies to slow the progression of cholangiopathies is limited, there is an urgent need for novel and effective medical treatment strategies," Trauner and colleagues wrote.
In their experiment, the researchers fed mice a diet enriched with 4% curcumin by weight for four and eight weeks. The mice were Mdr2-/-, a genetically altered strain that spontaneously develops progressive inflammatory conditions of the liver, including primary sclerosing cholangitis and primary biliary cirrhosis. These conditions can cause the liver bile ducts to become inflamed, scarred, and blocked, which leads to extensive tissue damage and fatal liver cirrhosis.

A control group of Mdr2-/- mice was fed a typical diet containing no curcumin. The researchers analyzed tissue and blood samples from the mice before and after adding curcumin to their diet. They found that curcumin reduced bile duct blockage and liver cell damage at both four and eight weeks by blocking portal myofibrocyte proliferation and decreasing expression of vascular cell adhesion molecule-1, thus reducing inflammation and fibrosis. No such delay in liver fibrosis was seen in the control group.
"These results show that curcumin may have multiple targets in liver, including activation of PPARgamma in cholangiocytes and inhibition of ERK1/2 signaling in portal myofibroblasts, thereby modulating several central cellular events in a mouse model of cholangiopathy," they wrote. "Targeting these pathways may be a promising therapeutic approach to cholangiopathies." They pointed out that curcumin might represent an alternative to ursodeoxycholic acid, the only current drug treatment for inflammatory liver disease, or liver transplant. The long-term effects of ursodeoxycholic acid remain unclear, they wrote, and curcumin might present a natural, well-tolerated option.
The study was funded by the Austrian Science Foundation and the Medical University of Graz. The authors reported that they had no financial conflicts of interest.
Spice in curry could prevent liver damage
Public release date: 29-Oct-2010
ST. LOUIS -- Curcumin, a chemical that gives curry its zing, holds promise in preventing or treating liver damage from an advanced form of a condition known as fatty liver disease, new Saint Louis University research suggests.

Curcurmin is contained in turmeric, a plant used by the Chinese to make traditional medicines for thousands of years.
SLU's recent study highlights its potential in countering an increasingly common kind of fatty liver disease called non-alcoholic steatohepatitis (NASH). Linked to obesity and weight gain, NASH affects 3 to 4 percent of U.S. adults and can lead to a type of liver damage called liver fibrosis and possibly cirrhosis, liver cancer and death.

"My laboratory studies the molecular mechanism of liver fibrosis and is searching for natural ways to prevent and treat this liver damage," said Anping Chen, Ph.D., corresponding author and director of research in the pathology department of Saint Louis University.

"While research in an animal model and human clinical trials are needed, our study suggests that curcumin may be an effective therapy to treat and prevent liver fibrosis, which is associated with non-alcoholic steatohepatitis (NASH)."

High levels of blood leptin, glucose and insulin are commonly found in human patients with obesity and type 2 diabetes, which might contribute to NASH-associated liver fibrosis.
Chen's most recent work tested the effect of curcumin on the role of high levels of leptin in causing liver fibrosis in vitro, or in a controlled lab setting.
"Leptin plays a critical role in the development of liver fibrosis," he said.
High levels of leptin activate hepatic stellate cells, which are the cells that cause overproduction of the collagen protein, a major feature of liver fibrosis. The researchers found that among other activities, curcumin eliminated the effects of leptin on activating hepatic stellate cells, which short-circuited the development of liver damage.

The findings were published in the September issue of Endocrinology.
Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: cancer, infectious disease, liver disease, aging and brain disease and heart/lung disease.

The Abstract

Curcumin Protects the Rat Liver from CCl4-Caused Injury and Fibrogenesis by Attenuating Oxidative Stress and Suppressing Inflammation

Yumei Fu, Shizhong Zheng, Jianguo Lin, Jan Ryerse and Anping Chen + Author Affiliations
Department of Pathology, School of Medicine, Saint Louis University, St. Louis, Missouri (Y.F., J.L., J.R., A.C.); and Research Institute of Chinese Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing, China (S.Z., A.C.)
Address correspondence to:Dr. Anping Chen, Department of Pathology, School of Medicine, Saint Louis University, 1402 S. Grand Blvd., St. Louis, MO 63104. E-mail:

We previously demonstrated that curcumin, a polyphenolic antioxidant purified from turmeric, up-regulated peroxisome proliferator-activated receptor (PPAR)-γ gene expression and stimulated its signaling, leading to the inhibition of activation of hepatic stellate cells (HSC) in vitro.

The current study evaluates the in vivo role of curcumin in protecting the liver against injury and fibrogenesis caused by carbon tetrachloride (CCl4) in rats and further explores the underlying mechanisms. We hypothesize that curcumin might protect the liver from CCl4-caused injury and fibrogenesis by attenuating oxidative stress, suppressing inflammation, and inhibiting activation of HSC.

This report demonstrates that curcumin significantly protects the liver from injury by reducing the activities of serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, and by improving the histological architecture of the liver.

In addition, curcumin attenuates oxidative stress by increasing the content of hepatic glutathione, leading to the reduction in the level of lipid hydroperoxide. Curcumin dramatically suppresses inflammation by reducing levels of inflammatory cytokines, including interferon-γ, tumor necrosis factor-α, and interleukin-6.

Furthermore, curcumin inhibits HSC activation by elevating the level of PPARγ and reducing the abundance of platelet-derived growth factor, transforming growth factor-β, their receptors, and type I collagen. This study demonstrates that curcumin protects the rat liver from CCl4-caused injury and fibrogenesis by suppressing hepatic inflammation, attenuating hepatic oxidative stress and inhibiting HSC activation.

These results confirm and extend our prior in vitro observations and provide novel insights into the mechanisms of curcumin in the protection of the liver. Our results suggest that curcumin might be a therapeutic antifibrotic agent for the treatment of hepatic fibrosis.

This work was supported by National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases grant R01-DK047995 (to A.C.).
Y.F. and S.Z. made equal contributions to this work.


Blueberry Ameliorates Hepatic Fibrosis, Study Finds

"In summary, in the present study, blueberries possessed a therapeutic effect on CCl4-induced hepatic fibrosis in rats through inhibiting liver inflammation and lipid peroxidation, and may be not related to the induction of phase-II enzymes through the activation of Nrf2 in rat liver during long-term of CCl4.

More detailed study is needed." see link below to full text.

ScienceDaily (June 17, 2010) - Conventional drugs used in the treatment of liver diseases inevitably have side effects. An increasing number of natural substances have been studied to explore if they have protective effects on the liver. Blueberries have unique effects on human retinal, brain and tumor cells, but reports about the effects of blueberries on liver diseases are lacking. A research article to be published on June 7, 2010 in the World Journal of Gastroenterology addresses this question. The research team led by Ming-Liang Cheng, MD, from Department of Infectious Diseases, Guiyang Medical College, Guiyang, presented some data from their research on the effectiveness of blueberries on liver fibrosis induced in laboratory animals.

Their study showed that blueberries could reduce liver indices, serum levels of hyaluronic acid and alanine aminotransferase, and increase levels of superoxide dismutase and decrease levels of malondialdehyde in liver homogenates compared with the model group. Meanwhile, the stage of hepatic fibrosis was significantly weakened. Blueberries increased the activity of glutathione-S-transferase in liver homogenates and the expression of Nrf2 and Nqo1 compared with the normal group, but there was no significant difference compared with the model group. The authors suggest that blueberry consumption is beneficial for hepatic diseases (including fibrosis). Journal Reference:Wang YP, Cheng ML, Zhang BF, Mu M, Wu J. Effects of blueberry on hepatic fibrosis and transcription factor Nrf2 in rats. World J Gastroenterol, 2010; 16 (21): 2657-2663 DOI:

Milk Thistle

Effects of Milk Thistle Extract on the Hepatitis C Virus Lifecycle

A laboratory study suggests that silymarin—an extract from the milk thistle plant—has multiple effects against the lifecycle of the hepatitis C virus. Hepatitis C is a chronic (long lasting) disease that primarily affects the liver and is often difficult to cure. The laboratory study examined the antiviral properties and mechanisms of silymarin on cultured (grown in a lab) human liver cells infected with the virus.

The study, funded in part by NCCAM, was published in the journal Hepatology.
The researchers grew human liver cells and infected them in vitro with the hepatitis C virus. The cells were then exposed to either standard hepatitis C drug treatment or to a diluted dose of silymarin. By analyzing the interactions between silymarin and the virus, the researchers observed that silymarin prevented the entry and fusion of the hepatitis C virus into the target liver cells..They also found that silymarin inhibited the ability of the

virus to produce RNA (a chemical that plays an important role in protein synthesis and other chemical activities of the cell), interfering with a portion of the virus's lifecycle. When measured against untreated cells, silymarin also significantly decreased viral load (the amount of virus in the cells), although to a lesser degree than treatment with interferon did. The researchers also found that silymarin prevented the cell-to-cell spread of the virus.

These findings build on previous research of silymarin's antiviral and anti-inflammatory properties and provide more information about the potential mechanisms involved in silymarin's antiviral actions. Further research, particularly in clinical trials, is needed to determine if silymarin could be a safe and effective supplement for treating hepatitis C in humans.

ReferenceWagoner J, Negash A, Kane OJ, et al.

The Study/Hepatology. 2010 Jun;51(6):1912-21.
Multiple effects of silymarin on the hepatitis C virus lifecycle.
Wagoner J, Negash A, Kane OJ, Martinez LE, Nahmias Y, Bourne N, Owen DM, Grove J, Brimacombe C, McKeating JA, Pécheur EI, Graf TN, Oberlies NH, Lohmann V, Cao F, Tavis JE, Polyak SJ.Department of Laboratory Medicine, University of Washington, Seattle, WA 98104-2499, USA.


Silymarin, an extract from milk thistle (Silybum marianum), and its purified flavonolignans have been recently shown to inhibit hepatitis C virus (HCV) infection, both in vitro and in vivo. In the current study, we further characterized silymarin's antiviral actions

Silymarin had antiviral effects against hepatitis C virus cell culture (HCVcc) infection that included inhibition of virus entry, RNA and protein expression, and infectious virus production..

Silymarin did not block HCVcc binding to cells but inhibited the entry of several viral pseudoparticles (pp), and fusion of HCVpp with liposomes. Silymarin but not silibinin inhibited genotype 2a NS5B RNA-dependent RNA polymerase (RdRp) activity at concentrations 5 to 10 times higher than required for anti-HCVcc effects

Furthermore, silymarin had inefficient activity on the genotype 1b BK and four 1b RDRPs derived from HCV-infected patients
Moreover, silymarin did not inhibit HCV replication in five independent genotype 1a, 1b, and 2a replicon cell lines that did not produce infectious virus..Silymarin inhibited microsomal triglyceride transfer protein activity, apolipoprotein B secretion, and infectious virion production into culture supernatants. Silymarin also blocked cell-to-cell spread of virus


Although inhibition of in vitro NS5B polymerase activity is demonstrable, the mechanisms of silymarin's antiviral action appear to include blocking of virus entry and transmission, possibly by targeting the host cell.

MID: 20512985 [PubMed - indexed for MEDLINE]

A double blind, placebo controlled study investigated the effects of a milk thistle extract vs. a placebo in a group of 50 children being treated with chemotherapy for acute lymphoblastic leukemia (ALL).
2009 Abstract

After 56 days of treatment, those using milk thistle “had a significantly lower AST and a trend toward a significantly lower ALT”, two liver enzymes used to measure hepatotoxicity.

In addition, Siliphos, the milk thistle extract used in the trial, didn’t counteract the effects of chemotherapy. It’s important to note that this was a preliminary investigation and researchers are urging subsequent research to determine the optimal dosage and duration of milk thistle treatment. Further inquiries need to establish whether the use of this herbal remedy will have any meaningful impact on survival outcome as well.A randomized, controlled, double-blind, pilot study of milk thistle for the treatment of hepatotoxicity in childhood acute lymphoblastic leukemia (ALL)

Elena J. Ladas MS, RD1, David J. Kroll PhD2, Nicholas H. Oberlies PhD3, Bin Cheng PhD4,
Deborah H. Ndao MPH1, Susan R. Rheingold MD5,

Kara M. Kelly MD1,*,

Article first published online: 14 DEC 2009
DOI: 10.1002/cncr.24723


Despite limited preclinical and clinical investigations, milk thistle (MT) is often used for the treatment of chemotherapy-associated hepatotoxicity. Limited treatment options exist for chemotherapy-related hepatoxicity. Given the wide use of MT, the authors investigated MT in both the laboratory and a clinical setting.

In a double-blind study, children with acute lymphoblastic leukemia (ALL) and hepatic toxicity were randomized to MT or placebo orally for 28 days.

Liver function tests were evaluated during the study period. To assess MT in vitro, the authors evaluated supratherapeutic concentrations in an ALL cell line.

Fifty children were enrolled. No significant differences in frequency of side effects, incidence and severity of toxicities, or infections were observed between groups. There were no significant changes in mean amino alanine transferase (ALT), aspartate amino transferase (AST), or total bilirubin (TB) at Day 28. At Day 56, the MT group had a significantly lower AST (P = .05) and a trend toward a significantly lower ALT (P = .07). Although not significantly different, chemotherapy doses were reduced in 61% of the MT group compared with 72% of the placebo group. In vitro experiments revealed no antagonistic interactions between MT and vincristine or L-asparaginase in CCRF-CEM cells. A modest synergistic effect with vincristine was observed.

In children with ALL and liver toxicity, MT was associated with a trend toward significant reductions in liver toxicity.

MT did not antagonize the effects of chemotherapy agents used for the treatment of ALL. Future study is needed to determine the most effective dose and duration of MT and its effect on hepatotoxicity and leukemia-free survival.

Cancer 2010. © 2009 American Cancer Society

Silymarin use and liver disease progression in the Hepatitis C Antiviral Long-Term Treatment against Cirrhosis trial.
Nov 2010

Alimentary Pharmacology & TherapeuticsN. D. Freedman 1, T. M. Curto 2, C. Morishima 3, L. B. Seeff 4, Z. D. Goodman 5, E. C. Wright 6, R. Sinha 1, J. E. Everhart 7, the HALT-C Trial Group 1Article first published online: 2 NOV 2010DOI: 10.1111/j.1365-2036.2010.04503.xPublished 2010.

This article is a US Government work and is in the public domain in the USA.

Author Information1 Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, MD, USA.2 New England Research Institutes, Watertown, MA, USA.3 Division of Virology, Department of Laboratory Medicine, University of Washington, Seattle, WA, USA.4 Division of Digestive Diseases and Nutrition, and Liver Diseases Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA.5 Division of Hepatic Pathology, Armed Forces Institute of Pathology, Washington, DC, USA.6 Office of the Director, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA.7 Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA.* Correspondence: Dr N. D. Freedman, Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd, EPS/320, MSC 7232, Rockville, MD 20852, USA. E-mail:


* Note: The terms "milk thistle" and "silymarin" are often used interchangeably.

Silymarin is the most commonly used herbal product for chronic liver disease; yet, whether silymarin protects against liver disease progression remains unclear.

To assess the effects of silymarin use on subsequent liver disease progression in 1049 patients of the Hepatitis C Antiviral Long-Term Treatment against Cirrhosis (HALT-C) trial who had advanced fibrosis or cirrhosis and had failed prior peginterferon plus ribavirin treatment.

Patients recorded their use of silymarin at baseline and were followed up for liver disease progression (two point increase in Ishak fibrosis score across baseline, year 1.5, and year 3.5 biopsies) and over 8.65 years for clinical outcomes.

At baseline, 34% of patients had used silymarin, half of whom were current users. Use of silymarin was associated (P more then 0.05) with male gender; oesophageal varices; higher ALT and albumin; and lower AST/ALT ratio, among other features. Baseline users had less hepatic collagen content on study biopsies and had less histological progression (HR: 0.57, 95% CI: 0.33–1.00; P-trend for longer duration of use=0.026). No effect was seen for clinical outcomes.
Silymarin use among patients with advanced hepatitis C-related liver disease is associated with reduced progression from fibrosis to cirrhosis, but has no impact on clinical outcomes

( #NCT00006164).

Caffeine in coffee reduces the severity of liver fibrosis in patients with chronic hepatitis C virus, as seen in the study below.
In August of 2010 data from a case-control study showed that: moderate coffee consumption significantly reduced the risk of HCC by almost half in chronic HBV.
In November of this year at the AASLD meeting in Boston a presentation evaluated the relationship between drinking coffee and the response to HCV anti-viral treatment .
The Conclusion: Pre-treatment coffee intake was independently associated with improved virologic response during peginterferon alfa-2a and ribavirin in the HALT-C trial.
"daily coffee consumption of 3 or more cups was associated with 25.8% SVR vs 20.7% for 1- less then 3 cups and 12.7% for less then 1 cup and these are all statistically significant. Coffee increased EVR & week20 responses too"
A study from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), published in the January 2010 issue of Hepatology; has shown that in people with chronic hepatitis C virus who drink about two and a quarter cups of coffee (with caffeine) daily had milder liver fibrosis. However, researchers found that other beverages containing caffeine did not have the same effects.
The Dec 8th 2010 Abstract below suggests greater than three cups of coffee is associated with reduced histological activity .

, Association Of Caffeine Intake and Histological Features of Chronic Hepatitis C.

J Hepatol. 210 Dec 8.

Costentin CE, Roudot-Thoraval F, Zafrani ES, Medkour F, Pawlotsky JM, Mallat A, Hézode C.

AP-HP, Service d'Hépatologie et de Gastroentérologie, Groupe Hospitalier Henri Mondor-Albert Chenevier, Créteil, 94000 France.

Rational The severity of chronic hepatitis C (CHC) is modulated by host and environmental factors. Several reports suggest that caffeine intake exerts hepatoprotective effects in patients with chronic liver disease.
The aim of this study was to evaluate the impact of caffeine consumption on activity grade and fibrosis stage in patients with CHC.
Methods 238 treatment-naı¨ve patients with histologically-proven CHC were included. Demographic, epidemiological, environmental, virological and metabolic features were collected, including daily consumptions of alcohol, cannabis, tobacco and caffeine during the six month preceding liver biopsy.
Daily caffeine consumption was estimated as the sum of mean intakes of caffeinated coffee, tea and caffeine-containing sodas.
Histological activity grade and fibrosis stage were scored according to Metavir. Patients (154 men, 84 women, mean age: 45±11 years) were categorized according to caffeine consumption quartiles: group 1 (less then 225 n="59)," n="57)," n="62)" more then 678 mg/day, n=60).
There was a significant inverse relationship between activity grade and daily caffeine consumption: Activity grade more then A2 was present in 78%, 61%, 52% and 48% of patients in group 1, 2, 3 and 4, respectively (p less then 0.001). more then A2 (OR=0.32 (0.12-0.85)).
Caffeine intake showed no relation with the fibrosis stage.
Caffeine consumption greater than 408 mg/day (3 cups or more) is associated with reduced histological activity in patients with CHC. These findings support potential hepatoprotective properties of caffeine in chronic liver diseases.

Copyright © 2010. Published by Elsevier B.V.
PMID: 21145804
[PubMed - as supplied by publisher]

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