Logical Fallacies Used Against HIV/AIDS Rethinkers or Dissidents
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Appeal to Popularity (argumentum ad populum)

Definition:
A proposition is held to be true because it is widely held to be true
or is held to be true by some sector of the population.

Example:
Everyone knows HIV causes AIDS, so why do you persist in your
outlandish claims?

Argument from Ignorance (argumentum ad ignorantiam)

Definition:

Arguments of this form assume that since something has not been
proven false, it is therefore true. Conversely, such an argument may
assume that since something has not been proven true, it is therefore
false. (This is a special case of a false dilemma, since it assumes
that all propositions must either be known to be true or known to be
false.)

Example:
Since you cannot prove that HIV does not cause AIDS, HIV causes
AIDS.

Appeal to Consequences (argumentum ad consequentiam)

Definition:
The author points to the disagreeable consequences of holding a
particular belief in order to show that this belief is false.

Example:
If you don't believe HIV causes AIDS, you're going to die of AIDS.

Appeal to Authority (argumentum ad verecundiam)

Definition:
While sometimes it may be appropriate to cite an authority to support
a point, often it is not. In particular, an appeal to authority is
inappropriate if:

(i) the person is not qualified to have an expert opinion on the
subject, (ii) experts in the field disagree on this issue.
(iii) the authority was making a joke, drunk, or otherwise not being
serious

Example:
Thousands of scientists agree there is overwhelming evidence that HIV
causes AIDS.

Fallacy of Exclusion

Definition:
Important evidence which would undermine an inductive argument is
excluded from consideration. The requirement that all relevant
information be included is called the "principle of total evidence".

Example:
Healthy HIV positive people who have never taken HIV/AIDS medications
are not included in many of the studies HIV/AIDS proponents cite as
evidence that HIV causes AIDS.

Coincidental Correlation (post hoc ergo propter hoc)

Definition:
The name in Latin means "after this therefore because of this". This
describes the fallacy. An author commits the fallacy when it is
assumed that because one thing follows another that the one thing was
caused by the other.

Example:
Jack came down with pneumonia after an HIV positive test result.
Therefore, Jack's pneumonia is AIDS caused by HIV because he tested
HIV+.

Begging the Question ( petitio principii )

Definition:
The truth of the conclusion is assumed by the premises. Often, the
conclusion is simply restated in the premises in a slightly different
form. In more difficult cases, the premise is a consequence of the
conclusion.

Example:
HIV causes AIDS because the evidence is overwhelming that HIV causes
AIDS. Therefore, HIV causes AIDS.



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Fundamental Failings, Flaws in the 'HIV/AIDS' Construct
=============================================
Flaw No.1: Co-Causal Factors Ignored

In order to assemble the HIV/AIDS construct, virologists had to make
a point of ignoring the prevalent, tangible causal factors for AIDS
and the absense of sexual contact between the cases they were
starting to see.

They then had to abuse genetic technology, exploiting the prestige of
its techniques in order to present a fa?de of credibility. The origin
of HIV/AIDS is not Africa, it is the abuse of genetic technology. We
only got HIV/AIDS when the technology arose to construct it. Science
was subsumed by technology. We know that anti-HIV drugs destroy T-
cells ( see this index of CD4 T-cells: What Do They Count For?
http://healtoronto.com/cd4counts.html
) and even the establishment
were forced to admit that HIV does NOT kill T-cells, at least not
directly, and the variety of other co-causes for T-cell depletion.

Although there is a shortage of studies examining the effects of
antiretroviral drugs upon CD4 cells, what we do have provides grounds
for saying that they definitely do destroy CD4 cells, that the effect
is predominantly a long term usage outcome and is most likely due to
cumulative mitochondrial damage. There are many references relating
to recreational drugs cytoxic effect.

And we also know that antiretroviral drugs destroy mitochondria
(Lewis et al. Mitochondrial toxicity of Antiretroviral Drugs, Nature
Medicine, Vol. 1, No. 5, pp 417-422, 1995). CD4 cells contain
mitochondria. We would expect the effects of mitochondrial toxicity
to be accentuated in CD4 T-cells because their rapid turnover renders
them more prone to cumulative mitochondrial DNA damage.

AZT has been found in several studies to be toxic to CD4 cells
(Balzarini et al. Journal of Biological Chemistry Vol. 264, pp 6127-
6133, 1989; Mansuri et al. Antimicrobial Agents and Chemotherapy Vol.
34, pp637-641, 1990; Hitchcock et al. Antiviral Chemistry and
Chemotherapy, Vol 2, pp 125-132, 1991.) An independent study showed
that AZT is about 1000-times (!) more toxic for human T-cells in
culture (at about 1 ÁM concentration) than the study conducted by its
manufacturer and the NIH concluded (Avramis et al, AIDS, Vol. 3, pp
417-422). Lymphocyte counts decreased significantly in humans treated
with AZT but not in untreated controls (Richman et al, NEJM, Vol. 317
pp 192-197, 1987) Another study found that AZT users experienced more
rapid CD4 cell depletion than those not on antiretrovirals (Alcabes
et al, American Journal of Epidemiology, Vol. 137, pp 898-1000, 1993).
Didanosine (ddI or Videx), is listed in the Physician's Desk Reference
(1999) as causing serious levels of "leukopenia" which involves
reductions of all white blood cells including lymphocytes in 13% to
16% of users.

In the June 2, 2002 issue of the Journal of Virology, researchers
report that the protease inhibitor drugs Crixivan (indinavir) and
Invarase (saquinavir) caused T cell death in healthy HIV negative
donor blood in three separate experiments:

http://healtoronto.com/tcelldeath.html


Immunology Today 1998 Vol.19 p 10-17 entitled "HIV-induced decline in
blood CD4/CD8 ratios: viral killing or altered lymphocyte
traffiking?" To quote from the article:

"During HIV infection CD4 cell numbers and CD4/CD8 ratios decline in
the blood. This is usually attributed to direct viral killing or to
other indirect mechanisms.

However, current models generally assume that such changes in the
blood are representative of changes in total CD4 T-cell numbers
throughout the body.

This article discusses the importance of alterations in CD4 and CD8
cell migration in regulating blood lymphocyte levels and questions
the extent of virus mediated CD4 T-cell destruction"

To also quote from Roederer, Nature Med. Vol 4 p145:

"In this issue of Nature Medicine, reports by Pakker et al and
Gorochov et al provide the final nails in the coffin for models of T-
cell dynamics in which a major reason for changes in T-cell numbers
is the death of HIV infected cells."

Flaw No.2: No Isolation or Validation

Any scientist who declares that a genetic sequence, moreover a
genetic sequence arrived at by human concensus, represents a naturally
occuring virus, has compromised their scientific integrity. To further
suggest that this genetic sequence represents a competent, exogenous,
sexually transmitted and indeed pathogenic retrovirus is to enter the
realms of pseudo-science. Without HIV isolation all is mere
speculation. Even if HIV were isolated and the proteins tested for by
the ELISA antibody test were actually proteins specific to HIV, an
antibody test would still not be accurate enough for determining
actual viral infection. Everyone tests HIV positive on ELISA if their
serum is not diluted by a factor of 400 because of non-specific
antibodies which bind to any proteins.

VIRAL ISOLATION INDEX
http://healtoronto.com/hiviso.html


Flaw No.3: Mutation

Any biological entity that mutates to the degree that HIV is said to
do cannot be biologically viable. For example "HIV protease" has to
make a large number of cleavages in the "HIV" gag-pol polyprotein in
order to produce biologically viable HIV. Kinetic analysis (J. of
Biological Chemistry, 1997, Vol. 272, p 6348-6353) shows that a
mutated HIV protease could not do this.

The idea with evolution by natural selection is that organisms
improve themselves by random mutations preserved by natural selection.
So, if a mutation confers an advantage it is preserved and the
organism is optimised for survival. When mutations confer a
disadvantage they are selected against because the organism carrying
this unfortuate mutation cannot persist in the population. If we are
talking about HIV as a viable biological entity then always the
fittest virions will comprise the greatest proportion of any
particular HIV population. Natural selection dictates that beneficial
mutations are PRESERVED. The basic message is that viral populations
can tolerate "high" levels of mutation as long as they are not so
high that beneficial mutations cannot be preserved in the majority of
the viral population.

We are being asked to believe that HIV is so prone to mutation as to
become simultaneously resistant to a combination of 3 anti-retroviral
agents and that despite this level of mutation HIV can still sustain
itself as a pathogenic virus.

If we assume that HIV does not mutate to an extent that renders it
naturally harmless (it is harmless anyway) then it will have
optimised its activity through natural selection. When exposed to an
unnatural inhibitor designed to block its HIV protease, the protease
will mutate to become resistant but because of the high precision
required of the protease in its function, infectious HIV cannot be
produced. To quote Dissident Scientist Dave Rasnick, PhD and former
designer of PIs or Protease Inhibitors from an article:

"Since the wild-type HIV protease has evolved to the optimal level of
activity, virtually all alterations to the enzyme's structure that
affect catalytic efficiency are lethal to the virus. Mutations of the
protease that reduce inhibitor binding result in an even more
profound reduction in catalytic activity. This is because the overall
catalytic efficiency of a mutant HIV protease is given by the product
of the relative efficiencies of the mutant enzyme with respect
to the wild-type for all eight obligatory cleavages (28) . These eight
cleavages can be thought of as an eight-number combination lock. Not
only does HIV protease have to make all eight cleavages, but the
enzyme must do it in the right order.

Therefore, even in the absence of inhibitors, the inhibitor-resistant
mutant HIV proteases do not lead to viable, infectious virus."

The latest questionable trend in AIDS research, drug resistance
testing deserve close scrutiny. Recent reports of growing numbers of
socalled "drug resistant" HIV positives have inspired sensational
media stories, calls for new drug development, and warnings that
unsafe sex is on the rise, effectively rallying public support for
more funding and more focus on AIDS.

I wonder how these tests can work if no actual HIV isolates are used
in the process. I also wonder why the AIDS Apologists assume that HIV
positives who have never taken AIDS meds and show drug resistance
must be having unsafe sex with HIV positives who are on the
treatments. Why not consider that resistance tests are flawed if they
show drug resistance in people who've never taken the drugs?

Flaw No.4: Viral Load

Polymerase Chain Reaction - PCR - or the 'viral load' test, purports
to detect, and quantify, blood-borne HIV in patients. However, the
genetic fragments it amplifies have never been proved to originate in
HIV, or in any virus. The accuracy of PCR viral load is estimated by
leading doctors at plus or minus 300% - i.e. a reading of 90,000
could be 30,000 or 270,000!

The PCR was not invented for HIV. Its Nobel Prizewinning inventor, Dr
Kary Mullis, calls the use of PCR in AIDS medicine, "a tragedy in the
practice of Western medicine." He says it is a misapplication of his
technology and measures genetic fragments or debris.

The uncertain unvalidated nature of the PCR for HIV is reflected in
the product literature supplied by manufacturers. A typical example
reads:

"The Amplicor HIV-1 Monitor test is not intended to be used as a
screening test for HIV or as a diagnostic test to confirm the
presence of HIV infection." - Roche, Amplicor

VIRAL LOAD OF WHAT?
http://www.virusmyth.net/aids/data/chjppcrap.htm


It hardly matters if PCR can accurately detect an arbitrary set of
RNA bases when no one has shown that that set causes any problems
like immune deficiency.

The fact that bacteria are replicated by RNA and DNA sequences means
nothing about their virulence. They replicate anything you stick in
there, that's what they do.

So, even if it came from outside the body[exogenous or non-naturally
occuring when most retroviruses are known to be endogenous or
naturally occuring as a part of all of our genetic make-up], that
still doesn't mean it is still there when the tests can't find it
anymore. Perhaps it is a parasite that was killed. It is no longer
there. Maybe your body produces antibodies to parasites and they
remain even after the parasites have been killed.

Dr. 'Hit Em Hard, Hit Em Early' Ho's viral load theory is merely a
mathematical model. It has no scientific foundation whatsoever. Even
establishment HIV scientists admit this now, see Nature Medicine,
1998, Vol 4, No.2, p 145-146. Viral load was just more technological
subterfuge to disguise the fact that "HIV" could never be found in HIV
positive people in numbers sufficient to cause disease.

Flaw No.5: Absence of Controls

The claims made by the AIDS establishment are simply not supported by
properly controlled, statistically significant studies. Here are some
examples of critically important controls for which the required
substantive studies do not exist despite the enormous amounts of
money given to AIDS research:

Prevalence of positive "viral load" in HIV negatives.

Comparison of CD4 T-cell counts over a long period between a group of
HIV negatives and a group of healthy, heterosexual HIV positives who
lead a healthy lifestyle (do not take recreational drugs, AIDS drug
cocktails, etc.).

Perfectly healthy people have been pushed onto the combos either as a
result of the "hit hard, hit early" doctrine or as a result of
indirect markers like viral load and CD4 count. There is no
comparison of survival times in developed countries of healthy HIV+
heterosexuals who lead a healthy lifestyle and were not given combos
for either of these reasons, with those in the same group who
were given them for these reasons.

Apart from the early fraudulent AZT trials and the damning Concorde
study (172 participants died, 169 while taking AZT, 3 while on
placebo) all studies of drug efficacy compare drugs with drugs, there
are no unmedicated controls.

Flaw No.6: Mechanism

HIV theory contradicts basic viological knowledge. Retroviruses
require cell proliferation for their propagation not cell death. They
do not kill cells.

In the early days of the HIV era a small group of virologists to
which everyone deferred stated as fact that HIV causes AIDS by
directly destroying CD4 cells, although there was no evidence for
this at the time.

When there was still no evidence, rather than follow the scientific
method and consider the importance of other factors, it was
confidently stated as fact that HIV instead causes AIDS by INDIRECTLY
destroying, or indirectly reducing, the number of CD4 cells. True to
form, there is still no evidence to clarify this position. Even after
receiving mind bogglingly huge research funding for over 21+ years
HIV 'scientists' or 'specialists' still do not have the evidence to
show how the putative 'HIV' can cause the catch-all condition called
'AIDS.'