Then where are the following 29 articles wrong please anaylize them one at a
time and post your evidence as to why a particular article is mistaken in
it's premises about Hep C.

NATAP - http://www.natap.org

29 RECENT HEPATITIS C ARTICLES posted to NATAP website:
http://www.natap.org

1. New Hep C Protease Inhibitor - (09/21/05)
http://www.natap.org/2005/HCV/092105_01.htm

2. Liver Injury and Changes in Hepatitis C Virus (HCV) RNA Load
Associated with Protease Inhibitor-Based Antiretroviral Therapy for
Treatment-Naive HCV-HIV-Coinfected Patients: Lopinavir-Ritonavir versus
Nelfinavir - (09/21/05)
http://www.natap.org/2005/HCV/092105_02.htm

3. PEGINTERFERON a-2b THERAPY IN ACUTE HEPATITIS C: IMPACT OF ONSET AND
DURATION OF THERAPY ON SUSTAINED VIROLOGIC RESPONSE - (09/20/05)
http://www.natap.org/2005/HCV/092005_01.htm

4. Fatigue & Hypermetabolism in HCV: high HCV RNA may cause fatigue &
interferon appears to reduce fatigue - (09/19/05)
http://www.natap.org/2005/HCV/091905_03.htm

5. HCV natural history in the west & developing world: The retrospective
and prospective in perspective - (09/19/05)
http://www.natap.org/2005/HCV/091905_02.htm

6. (Marijuana/Hash) Endocannabinoids and liver disease - review -
(09/19/05)
http://www.natap.org/2005/HCV/091905_01.htm

7. Impact of Hepatitis C Virus on Immune Restoration in HIV-Infected
Patients Who Start Highly Active Antiretroviral Therapy: A Meta-analysis -
(09/14/05)
http://www.natap.org/2005/HCV/091405_10.htm

8. Hepatitis C Virus Infection in HIV Type 1-Infected Individuals Does
Not Accelerate a Decrease in the CD4+ Cell Count but Does Increase the
Likelihood of AIDS-Defining Events - (09/14/05)
http://www.natap.org/2005/HCV/091405_09.htm

9. VA Study: HCV Increases Risk of Death Among HAART-Treated HIV+
Patients by 30-80% - (09/14/05)
http://www.natap.org/2005/HCV/091405_08.htm

10. Influence of Hepatitis C Virus Infection on HIV-1 Disease
Progression and Response to Highly Active Antiretroviral Therapy -
(09/14/05)
http://www.natap.org/2005/HCV/091405_07.htm

11. Hepatic steatosis with stavudine in HIV/hepatitis C virus
co-infection - (09/14/05)
http://www.natap.org/2005/HCV/091405_06.htm

12. Promising Therapy for Human Hepatoma (liver cancer, HCC): Telomerase
Inhibition by GRN163 - (09/13/05)
http://www.natap.org/2005/HCV/091405_05.htm

13. Single (B or C), dual (BC or BD) and triple (BCD) viral hepatitis in
HIV-infected patients in Madrid, Spain - (09/13/05)
http://www.natap.org/2005/HCV/091405_04.htm

14. Is Cirrhosis Inevitable in HCV? - (09/13/05)
http://www.natap.org/2005/HCV/091405_03.htm

15. Insulin resistance is a cause of steatosis and fibrosis progression
in chronic hepatitis C - (09/13/05)
http://www.natap.org/2005/HCV/091405_01.htm

16. Hepatocellular carcinoma in 40 HIV/HCV-coinfected versus 50
HCV-monoinfected patients. North American HCC in HIV Study Gro (09/09/05)
http://www.natap.org/2005/ias/ias_53.htm

17. Caucasians Had Better HCV Viral Load Reductions Than
African-Americans During First 3 Days & During Weeks 1-4 After Starting
Peg/RBV (09/09/05)
http://www.natap.org/2005/ias/ias_52.htm

18. Hepatitis C infection is not associated with systemic HIV-associated
non-Hodgkin's lymphoma: a cohort study (09/09/05)
http://www.natap.org/2005/ias/ias_51.htm

19. PI & NNRTI Drug Levels in Coinfected Patients (09/09/05)
http://www.natap.org/2005/ias/ias_50.htm

20. Pegasys/RBV Improves Histology in Non-Responders & Cirrhotics
(09/09/05)
http://www.natap.org/2005/ias/ias_49.htm

21. PegIFN/RBV May Be Less Effective in Acute HCV for HIV+ (09/09/05)
http://www.natap.org/2005/ias/ias_48.htm

22. PK of Once Daily Regimen: Fosamprenavir/r, Tenofovir and FTC in
Naives (09/09/05)
http://www.natap.org/2005/ias/ias_47.htm

23. Occult HCV- HCV RNA Found in Liver of Patients Negative for
Antibody-HCV & Serum HCV RNA - (09/05/05)
http://www.natap.org/2005/HCV/090505_20.htm

24. EDITORIAL COMMENTARY Hepatitis C Virus (HCV) Occult Infection or
Occult HCV RNA Detection? - (09/05/05)
http://www.natap.org/2005/HCV/090505_10.htm

25. HCV Did Not Persist in Patients with SVR - (09/05/05)
http://www.natap.org/2005/HCV/090505_19.htm

26. Divining the role of liver biopsy in hepatitis C - (09/05/05)
http://www.natap.org/2005/HCV/090505_18.htm

27. Chronic hepatitis C and 'normal' ALT levels: Treat the disease not
the test - (09/05/05)
http://www.natap.org/2005/HCV/090505_17.htm


28. Gilead, Achillion initiate phase I trial evaluating GS 9132 for
treatment of hep C - (09/05/05)
http://www.natap.org/2005/HCV/090505_16.htm

29. Isatoribine, an agonist of TLR7, reduces plasma virus concentration
in chronic hepatitis C infection - (09/05/05)
http://www.natap.org/2005/HCV/090505_15.htm

If that's not enough for you there are 420 more articels posted at the
following URL;
http://www.natap.org/hcv.htm

Gary Stein

You forget, Gary.
There is a massive global biomedicalconspiracy that has infiltrated
every single academic institute, every hospital and every research
laboratory. All employees are co-conspirators paid directly or
indirctly by BigPharma to create non-existent organisms and diseases.
Of course you will see thousands of studies on Hepatits C - but none of
them were really carried out, and all are fraudulent.

You forget, Gary.
There is a massive global biomedicalconspiracy that has infiltrated
every single academic institute, every hospital and every research
laboratory. All employees are co-conspirators paid directly or
indirctly by BigPharma to create non-existent organisms and diseases.
Of course you will see thousands of studies on Hepatits C - but none of
them were really carried out, and all are fraudulent.

No conpiracy required. There is little incentive to question existing
dogma, even if it was not properly established in the first place
(using controlled, double-blinded experiments, for example).

There are many scientific models that coexist, yet one must be correct,
or at least more accurate, than the other. Those who don't examine the
points made by the Perth Group, for example, are not doing science,
which requires that all scientific challenges be taken seriously. A
hypothesis is supposed to be scrutinized; otherwise, we would still
believe in a flat earth.

As an example of a what is going on all the time (though the public is
not aware of it), the following report is from TODAY. There are
similar examples all over the place. Go to www.gilbertling.org and
read about how he has tried to get funding for more experiments to
clarify his A-I hypothesis, but because a bureaucrat does not like him,
the experiments are not getting done.

Wake up and smell the coffee, people!

9/24/2005
"Sugar Helps Control Cell Division"

"...The dogma for decades has been that the cycle of cell division is
controlled by the appearance and disappearance of certain proteins
called cyclins, but experiments have shown that you can knock out any
of these and still get perfectly normal cell division..."

Source: www.sciencedaly.com


The other intesting thing is that there really is no "HIV/AIDS
hypothesis," because it varies from one period of time to another and
from one place to another. Let's start with exactly what the
hypothesis is, otherwise, there can be no scientific debate. Most
people in the USA (including doctors) think that after infection, a
person will live several years, perhaps a decade or so, then die of
"immune system failure," yet there is the following:

"Less than a quarter of HIV-positive men with haemophilia in the United
Kingdom are still alive 20-25 years after infection with HIV,"
So over 20% of people who are already very ill people can live over 25
years or so with HIV.

And then: "... liver disease has become the major cause of death
amongst HIV-positive men with haemophilia."

This is not an "AIDS defining illness," nor has anyone suggested it is.

How is this possible? What is the hypothesis, exactly?

Source: Sabin C et al. Twenty five years of HIV in haemophilic men in
Britain: an observational study. BMJ, September 16th, 2005 (online
edition).

I have accepted my version of the Duesberg challenge, but nobody wants
to take me up on it, so they don't even believe in their own nonsense.

Then I asked, hypothetically, if someone did take me up on the
challenge, what would you inject me with? I will only allow "pure
virus" and an inert susbstance in which to suspend the virus. How are
you going to obtain this virus, since it was never isolated? How will
you isolate it, exactly? Explain it. Only fragments, either of the
wrong size and right shape (according to the dogma, anyway) or of the
correct size and wrong shape, have ever been found, and they are most
likely from humans cells that destroyed in the massive oxidative stress
that actually does cause most of what is called "AIDS" these days (in
the USA, at least).

No conspiracy, just stupidity, fear of reprisals and loss of grants,
greed, etc. - all the things that make us human.

So take me up on the Duesberg challenge, or we could agreee upon a Hep
C challenge. How, exactly, are you going to isolate this "Hep C
virus?" If you beleive in a virus, isolate it and let's talk about
doing a experiment that will determine who is correct. The problem, of
course, is that you cannot isolate what is not present.

Even true believers have to admit the nonsense, though they do it in a
quiet way:

"...the virus has not been grown in tissue culture. Thus, basic studies
of the virus are not possible and studies are limited to gene
sequencing and clinical studies. and clinical studies..."

Source: http://www.hepnet.com/hkn/c11.html

Do you people understand the implications of this? Why can't they grow
it? There is no reason, except that it does not exist!

They say: " The virus for hepatitis C was cloned in 1989," but what
does this mean, exactly? Again, fragments were found that most likely
were part of human cells that underwent tremendous stress and died off.
These fragments were cloned and said to be "Hep C." Why? So that a
big company could make big money. Does that surprise you? Is it the
first example in human history of a company claiming something that is
not likely true in order to make huge profits? Do you think everyone
in the company understand exactly what is going on at the molecular
level? Let's be real now! You are the ones with the naive view of
humanity.

The "studies" that allegedly support the virus claim are circular logic
- they assume a virus. In science, you cannot assume what you seek to
demonstrate. That is what religious debate is often like, for example,
assuming the Bible is the word of God, when there is no way to know
that scientifically. So of course the studies will appear to support
the virus idea. Do they compare this claim to an oxidative stress
hypothesis? Find me a citation that answers that question.

I have confidence that I could "cure" "Hep C" in an animal model, but
these clowns admit that they have not been able to create one for "Hep
C," which is a damning statement by itself. In people, we are dealing
with "patients" who have done tremendous damage to themselve, and who
usually don't listen to any authorities, let alone those who have no
power to enforce their demands (such as doctors), which is why I offer
myself up to demonstrate that this is all nonsense. However, because
there is no virus, there is no way for anyone to take me up on my
offer, even if they were naive enough to do so.

On 22 Sep 2005 14:46:09 -0700, "montygram" <nazztrader@lycos.com>
wrote:

Hey, aren't you the guy that says no one should EVER even sniff an
omega-3 fatty acid?

Thank you, Mr. Stein, for presenting these 29 articles on Hep-C. Hey!
That's neat: One for every indicator disease of AIDS! What a
coincidence!
Of course, I'll need a little time to study them, in order to find out
what's wrong with them.
There's no doubt, of course, that there IS something worng with them,
because Hep-C Virus doesn;'t exist. There is no record of it being
isolated. Some hepatic disease agency in this country informed me that
there are 9 classes of HCV and more than 100 subclasses. But they gave me
absoluely zero information on the physical properties of this 'virus' Not
even one puny subclass.
Of course they need this many different forms of the virus, because they
have to explain away all the different discrepancies of the virus model,
and one single virus type couldn't possibly do that.
There is another theory that explains all the deaths from liver disease
very well: Hepatic damage from all the toxic drugs that are being used to
fight that other non-existing virus: HIV.
HCV is the "Alibi Virus", so to speak.
But don't go away; I'll be back when I've read those papers.

In article <1127425569.781911.7580@g14g2000cwa.googlegroups.c om>,
montygram <nazztrader@lycos.com> wrote:
The expectation for *U*N*T*R*E*A*T*E*D* people with HIV infection is
that about half develop AIDS within a decade.

These people are being treated.

--
David Canzi "I am not denying anything." -- Celia Farber

Nobody remembers... conspiracies are more interesting!

Oh puhlease!! Here comes Paper #1:

who were nonresponders to peginterferon + ribavirin combination therapy.
It is important to note that these Phase 1 studies were conducted with a
capsule formulation that is viable for larger-scale clinical studies and,
potentially, for commercial development."

It says nothing about Hep-C, the virus. It just ASSUMES that's the
problem. Schering Plough is plotting a new poison, to be used on hapless
patients who have already been half-killed by peginterferon+ribavirin.
Ribavirin is a terrible toxin. It's main side effect is hemolytic anemia
(= forced apaoptosis of red blood cells) Brrrrr!

Tadaaaaa! Her comes paper #2:

weighing <60 kg received 30 mg). All subjects were screened for HCV by
means of an HCV ELISA. Seventy (11%) of 653 subjects enrolled in the
parent clinical trial were HCV-antibody reactive upon HCV ELISA testing.

".....this analysis confirms that HCV loads increase after HAART
initiation and that this increase is associated with appropriate immune
reconstitution. These increases may be accompanied by flares in the ALT
level."

<Sob!> The same old shit as with 'HIV' ! Testing with ELISA, this time
with proteins ASSUMED to come from 'HCV'. Also Viral Load testing while
at the same time murdering the patient with lamivudine and stavudine.

Any evidence of Hep-C Virus? I'm not seeing it.

Paper #3 is about monotherapy with Peginterferon a-2b:

spontaneously before therapy. 79 subjects with persistent viremia were
randomized to 3 groups (Table). The end of treatment response was 94% and
the overall SVR was 82%. The SVR was better for genotype 4 compared to
genotype 1. Earlier treatment (week 8 or 12) was associated with higher
SVR particularly in genotype 1. Twelve week therapy was sufficient for
genotype 4 while higher SVR rates in genotype 1 patients were achieved
with 24 wks treatment (86%). Peginterferon c~-2b monotherapy was well
tolerated and associated with significant improvement in the quality of
life."

These genotypes depend on what kind of genetic sludge has been used to
prime the PCR.
Peginterferon a-2b is well-tolerated. As a monotherapy it will not kill
you as easily as in combination with Ribavirin. I can believe that.
But just waiting until the condition clears up by itself, as happened to 9
subjects, works too.

Paper #4:

resting energy expenditure (REE) increases during chronic hepatitis C is
not known. Our aims were: (a) to determine the metabolic state of patients
with chronic hepatitis C, and (b) to evaluate the effects of interferon
therapy on REE.

Well, this study came out the same way it always happens in the clinic:
Some patients respond to treatment, other patients don't.

But wait: The authors claim that the REE is really caused by the virus
(HCV):

result of HCV replication rather than the consequence of hepatic
inflammation."

Yeah, it might... Now if we could only prove that there IS a virus...
Hm! Viral load, eh? Isn't that based on quantitative PCR? What did kary
Mullis have to say about that?

Paper #5 is very exciting. To marketing people, that is, not to
scientists:

whom may be coinfected with HIV and/or HBV and have very limited access to
treatment. Even if only 10% of such individuals advanced to cirrhosis, the
global burden of this infection is staggering. Thus HCV, like HIV, is a
disease of two worlds, one where new infections are rare and effective
treatments are available and one where high population density, inadequate
preventive strategies and inaccessible treatments maintain HCV as a common
disease with devastating consequences."

Now if you read that, doesn't it give you an idea that there's money to be
made?
This "natural history of HCV" nowhere mentions when or where 'HCV' was
discovered or isolated. It just enters the story unobtrusively.
Suddenly, it's there.
I agree with one point: HCV is like HIV.

5 sets of personal opinions completely devoid of any discussion of facts
don't an argument make Herr Doctor Iconclaster....

Gary Stein

"Iconoclaster" <wgods@xs4all.nl> wrote in message
news:2843ece1789d5b7f5d8fd3f5429c5a31@localhost.ta lkabouthealthnetwork.com...

On Sat, 24 Sep 2005 20:10:21 -0400, "Iconoclaster" <wgods@xs4all.nl>
wrote:
snip
You haven't looked for it and wouldn't know what to do if the evidence
was staring you in the face. At best, you live in a world of
technology that has not gotten passed about 1938.

NOTHING in ANY of your posts suggests that your unsujpported opinion
should be given more attention than a rat's fart.

George M. Carter

Mr. Stein, do you really mean to say that this paper makes any kind of
argument? The point we're discussing is the non-existance of HCV,
remember?

Not by you, Mr. Carter. But surely by people who are able to think for
themselves. You only have to read this paper to seen that it presents
absolutely no evidence in favor of the existance of HCV.

Paper #6: (Marijuana/Hash) Endocannabinoids and liver disease - review -

Well, this paper is exactly what the title says it is. But... NOT A WORD
ON HCV, or any virus at all.
It does contain the following stement:


Ouch! That will take away the chance for hippies and other babyboomers to
blame all the mysery on some real or imagined virus.

Paper #7: Impact of Hepatitis C Virus on Immune Restoration in
HIV-Infected Patients Who Start Highly Active Antiretroviral Therapy: A
Meta-analysis -

This is indeed a Meta-analysis, i.e., a literature search and comparison
of a number of papers on the subject. The authors note:

studies, the increase in the CD4 cell count was a secondary outcome, and
many of the studies are statistically underpowered to examine the specific
question of interest to us."

Nevertheless, the conclusion of this study is:

after 48 weeks of HAART, than do patients with HCV infection alone. "

The auhors don't come up with an explanation of this phenomenon.
My objection is that, again, "HCV infection" is taken for granted. Like
"HIV infection" it is based on an antibody test. As there is no standard
in the form of a pure HCV preparation (if there were, they would have
cited a reference), the term "HCV infection" has no real meaning.

Paper #8: Hepatitis C Virus Infection in HIV Type 1-Infected Individuals
Does Not Accelerate a Decrease in the CD4+ Cell Count but Does Increase
the Likelihood of AIDS-Defining Events

Well, the title says it all, now doesn't it?
If you've tested HIV+, you croak sooner if your liver is screwed up too,
and CD4+ cells have nothing to do with that. The paper states:

alone."

Note that these patients were treated with HAART. Their CD4+ cells went
up, but they died anyway of liver disease. This is a very clear example
where they sorely need another fantasy virus (HCV) to explain this
outcome!