> http://www.vancouversun.com/life/coffees+keep+liver+disease+Study/2132375/story.html
>
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>
> _______________________________________________________________
Gonna make a cup right now.
M
Cactus Jammies schreef:
> http://www.vancouversun.com/life/coffees+keep+liver+disease+Study/2132375/story.html
>
> - cactus jammies ( I drink about four cups of fresh ground coffee per day)
Coffee *actively endangers your treatment*, I will just quote the Hepc
Nomads Nurse:
First of all, the study said that the coffee drinkers also SMOKED more
and drank more alcohol.
one of the CYP450 enzymes, CYP1A2, is implicated in liver damage (and
tobacco related cancer)....and SMOKING INCREASES THE ACTIVITY OF THIS
ENZYME THREEFOLD!!!!! You know what else induces this enzyme? Caffeine.
So that alone speaks againt this study.
Second....coffee is associated with an increase in inflammatory
markers....the same markers that are elevated in Hep C patients.....
Associations between coffee consumption and inflammatory markers in
healthy persons: the ATTICA study
Antonis Zampelas, Demosthenes B Panagiotakos, Christos Pitsavos,
Christina Chrysohoou and Christodoulos Stefanadis
From the Department of Nutrition and Dietetics, Harokopio University,
Athens, Greece (AZ and DBP); and the First Cardiology Clinic, School of
Medicine, University of Athens, Greece.
Background: The effect of coffee consumption on the cardiovascular
system is conflicting. Inflammation is important to the development of
cardiovascular disease (CVD), and several dietary factors are thought to
exert significant effects on inflammation and thus on the risk of CVD.
Objective: We aimed to investigate the associations between coffee
consumption and inflammatory markers.
Design: The cross-sectional survey enrolled 1514 men ( ± SD age: 46 ± 13
y; range: 18–87 y) and 1528 women (aged 45 ± 13 y; range: 18–89 y). Five
percent of men and 3% of women were excluded for history of CVD. Fasting
blood samples were collected. Dietary habits (including consumption of
various types of coffee) were evaluated by using a validated
food-frequency questionnaire.
Results: Compared with coffee nondrinkers, men who consumed >200 mL
coffee/d had 50% higher interleukin 6 (IL-6), 30% higher C-reactive
protein (CRP), 12% higher serum amyloid-A (SAA), and 28% higher tumor
necrosis factor concentrations and 3% higher white blood cell (WBC)
counts (all: P < 0.05). Women who consumed >200 mL coffee/d had 54%
higher IL-6, 38% higher CRP, 28% higher SAA, and 28% higher tumor
necrosis factor concentrations and 4% higher WBC counts (all: P < 0.05)
than did coffee nondrinkers. The findings were significant even after
control for the interactions between coffee consumption and age, sex,
smoking, body mass index, physical activity status, and other covariates.
Conclusions: A relation exists between moderate-to-high coffee
consumption and increased inflammation process. This relation could
explain, in part, the effect of increased coffee intake on the
cardiovascular system.
---------------------
Third.....in prediabetics (those whose fasting blood sugar is above 100)
coffee causes an increase in insulin production of 17%. Prediabetics are
insulin resistant....which causes higher levels of insulin.....and you
add to that the 17% more insulin from coffee and what do you have?
HYPERINSULINEMIA.
And hyperinsulinemia.... increases HCV replication and blocks the
effects of interferon.....
Aren't those enough reasons to never buy coffee again?
Hyperinsulinemia Blocks The Inhibition Of Hepatitis C Virus (Hcv)
Replication By Interferon. A Potential Mechanism For Failure Of
Interferon Therapy In Subjects With Hcv And Nonalcoholic Fatty Liver
Disease.
Arun J Sanyal, Nisha Chand, Kevin Comar, Faridodin Mirshahi,
Virginia Commonwealth University, Richmond, VA
Background:
Hepatic steatosis and obesity are risk factors for failure of interferon
(IFN) therapy in subjects with HCV. Both obesity and fatty liver are
associated with the metabolic syndrome which is characterized by insulin
resistance and hyperinsulinemia. The effects of hyperinsulinemia on
IFN-mediated inhibition of HCV replication were unknown.
Hypothesis:
Hyperinsulinemia blocks the inhibition of HCV replication by IFN.
Specific Aims:
To examine the effects of insulin on IFN-mediated inhibition of HCV RNA.
Methods:
A commercially available HCV replicon system (Apath, Clone B(S1179I)
comprised of a Huh-7 hepatoma cell line stably transfected with full
length HCV RNA was used. The effects of varying concentrations of
insulin (0-128 uU/ml) on the anti-viral activity of alpha-IFN (50 LUlml)
were studied. The endpoints measured included: (1) HCV replication:
quantitative real-time PCR of HCV RNA, and (2) IFN-induced anti-viral
proteins: protein kinase R (PKR) and interferon regulatory factor-1
(IRF-1) (Western blot). The pathways by which insulin produced these
effects were evaluated by specific blockade of the phosphatidyl
inositol-3 kinase (PI3K) with LY 294002, and blockade of mitogen
activated protein kinase (MAPK) pathway with PD098059.
Results:
Following exposure to IFN for 30 minutes to 12 hours, there was a highly
significant (p< 0.001) decrease (mean + I - S.D.: -90 +I- 5%) in HCV
replication. Insulin alone had no substantial effects on HCV replication
at physiolgic concentrations (< 64 uUlml). However, at high insulin
concentrations (128 uUlml), there was a significant increase (31 +I- 8%,
p< 0.05) in HCV replication. While physiologic concentrations of insulin
had no effects on IFN-induced decrease in HCV RNA levels, there was a
marked blockade of IFN effects on
HCV RNA (-92 +/- 8% with IFN alone vs -33 + I - 10% IFN + insulin
compared to serum free media, P< 0.001) at [insulin]= 128 uU/ml. As
expected, IFN produced a mean 3.5 fold increase in both PKR and IRF-1
expression.
Insulin alone had no effects on the expression of either protein.
However, insulin blocked the IFN-mediated increase in PKR and IRF-1. The
effects of insulin on HCV RNA were almost completely blocked by LY
294002while PD 098059 did not produce a significant effect.
Conclusions:
Insulin, at concentrations seen in the insulin-resistant state,
increases HCV replication. Insulin also significantly blocks the
suppressive effects of interferon on HCV RNA. This effect is mediated by
the PI3K signal transduction pathway. Insulin also blocks the induction
of two major anti-viral proteins PKR and IRF by IFN which may contribute
to the effects of insulin on interferon-mediated suppression of HCV.

Signature
HCV Care group HepC Nomads: http://hepcnomads.co.uk/phpBB3/index.php
Waterspider unmasked
http://groups.google.com/group/alt.support.hepatitis-c/msg/987c5a3337fe148d?dmod
e=source
Cactus Jammies - 30 Oct 2009 19:13 GMT
Guffaw
cactus jammies
==============
> Cactus Jammies schreef:
>>
[quoted text clipped - 125 lines]
> anti-viral proteins PKR and IRF by IFN which may contribute to the effects
> of insulin on interferon-mediated suppression of HCV.
I drink about 4 cups a day too. Hallelujah! FINALLY, something I really
enjoy that's liver-friendly.
> http://www.vancouversun.com/life/coffees+keep+liver+disease+Study/2132375/story.html
> - cactus jammies ( I drink about four cups of fresh ground coffee per
[quoted text clipped - 75 lines]
> http://www.vancouversun.com/life/coffees+keep+liver+disease+Study/2132375/story.html
> _______________________________________________________________