Original Message:
-----------------
From: dshsfca@ixpres.com (D. Stephen Heersink)
Date: Mon, 30 Aug 2004 08:46:23 GMT
To: kjlandis@alumni.usc.edu
Subject: Re: In Search of HIV
On Fri, 27 Aug 2004 00:19:15 -0400, "KellyJonLandis"
<kjlandis@alumni.usc.edu> wrote:
Readers of this nonsense may be interested in an article extracted as
follows:
I agree with the article's premise, but do not feel you have made your
point that AIDS Dissidents are advancing pseudo-science or junk science
simply by your dismissive attitude and waving of the hand as you offered
up the ad hominem exclamation "nonsense" [ie: "nuh uh."]
Kelly Jon Landis
Readers of Stephen Heersink's dismissive, ad hominem comments may be even
more interested in the logical fallacies often used against AIDS
Dissidents and below that, failings in the 'HIV/AIDS' construct.
================================================== ==============
Logical Fallacies Used Against HIV/AIDS Rethinkers or Dissidents
================================================== ==============
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.
=============================================
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 µM 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.'
Mechanisms of delusion
Troubled science takes many forms, from pseudoscience (irrational or
mystical systems of thought dressed up in ostensibly scientific
jargon, often complex but never rigorous) to junk science
(methodologically sloppy research usually conducted to advance some
extrascientific agenda or to prevail in litigation) to outright fraud.
I am concerned here not with dishonest practices, which are rarely
intellectually interesting, but with serious investigations leading
down pathways that ultimately prove erroneous. As Nobel-winning
chemist Irving Langmuir said in his famous General Electric lecture on
the topic, "These are cases where there is no dishonesty involved, but
where people are tricked into false results by the lack of
understanding about what human beings can do to themselves in the way
of being led astray by subjective effects, wishful thinking, or
threshold interactions."2
The road to greater scientific truth is not just littered with
history's errors; it is built through a process of constant error
correction. If we accept Kuhn's description of scientific progress as
a succession of revolutions, or paradigm shifts, resulting from the
constant effort to reconcile new results with dominant paradigms, then
a scientific field's moments of crisis--when different factions
contend over whether an idea will turn out to be revolutionary or
absurd--tell us a great deal about how knowledge is constructed,
tested, and defended. For this reason, understanding pathological
science can help a researcher better understand, and perform, reliable
science.
Kind regards,
_____________________
D. Stephen Heersink
San Francisco
On Fri, 27 Aug 2004 00:19:15 -0400, "KellyJonLandis"
<kjlandis@alumni.usc.edu> wrote:
would call an independent assesment of the role of hiv, its isolation,
and the damage the hiv virus does to the immune system. Denial is very
high on the list of mental health problems some people face while
managing their hiv status
EVIDENCE THAT HIV CAUSES AIDS
HIV fulfills Koch's postulates as the cause of AIDS.
Among many criteria used over the years to prove the link between
putative pathogenic (disease-causing) agents and disease, perhaps the
most-cited are Koch's postulates, developed in the late 19th century.
Koch's postulates have been variously interpreted by many scientists,
and modifications have been suggested to accommodate new technologies,
particularly with regard to viruses (Harden. Pubbl Stn Zool Napoli
[II] 1992;14:249; O'Brien, Goedert. Curr Opin Immunol 1996;8:613).
However, the basic tenets remain the same, and for more than a century
Koch's postulates, as listed below, have served as the litmus test for
determining the cause of any epidemic disease:
Epidemiological association: the suspected cause must be strongly
associated with the disease.
Isolation: the suspected pathogen can be isolated - and propagated -
outside the host.
Transmission pathogenesis: transfer of the suspected pathogen to an
uninfected host, man or animal, produces the disease in that host.
With regard to postulate #1, numerous studies from around the world
show that virtually all AIDS patients are HIV-seropositive; that is
they carry antibodies that indicate HIV infection. With regard to
postulate #2, modern culture techniques have allowed the isolation of
HIV in virtually all AIDS patients, as well as in almost all
HIV-seropositive individuals with both early- and late-stage disease.
In addition, the polymerase chain (PCR) and other sophisticated
molecular techniques have enabled researchers to document the presence
of HIV genes in virtually all patients with AIDS, as well as in
individuals in earlier stages of HIV disease.
Postulate #3 has been fulfilled in tragic incidents involving three
laboratory workers with no other risk factors who have developed AIDS
or severe immunosuppression after accidental exposure to concentrated,
cloned HIV in the laboratory. In all three cases, HIV was isolated
from the infected individual, sequenced and shown to be the infecting
strain of virus. In another tragic incident, transmission of HIV from
a Florida dentist to six patients has been documented by genetic
analyses of virus isolated from both the dentist and the patients. The
dentist and three of the patients developed AIDS and died, and at
least one of the other patients has developed AIDS. Five of the
patients had no HIV risk factors other than multiple visits to the
dentist for invasive procedures (O'Brien, Goedert. Curr Opin Immunol
1996;8:613; O'Brien, 1997; Ciesielski et al. Ann Intern Med
1994;121:886).
In addition, through December 1999, the CDC had received reports of 56
health care workers in the United States with documented,
occupationally acquired HIV infection, of whom 25 have developed AIDS
in the absence of other risk factors. The development of AIDS
following known HIV seroconversion also has been repeatedly observed
in pediatric and adult blood transfusion cases, in mother-to-child
transmission, and in studies of hemophilia, injection-drug use and
sexual transmission in which seroconversion can be documented using
serial blood samples (CDC. HIV AIDS Surveillance Report 1999;11[2]:1;
AIDS Knowledge Base, 1999). For example, in a 10-year study in the
Netherlands, researchers followed 11 children who had become infected
with HIV as neonates by small aliquots of plasma from a single
HIV-infected donor. During the 10-year period, eight of the children
died of AIDS. Of the remaining three children, all showed a
progressive decline in cellular immunity, and two of the three had
symptoms probably related to HIV infection (van den Berg et al. Acta
Paediatr 1994;83:17).
Koch's postulates also have been fulfilled in animal models of human
AIDS. Chimpanzees experimentally infected with HIV have developed
severe immunosuppression and AIDS. In severe combined immunodeficiency
(SCID) mice given a human immune system, HIV produces similar patterns
of cell killing and pathogenesis as seen in people. HIV-2, a less
virulent variant of HIV which causes AIDS in people, also causes an
AIDS-like syndrome in baboons. More than a dozen strains of simian
immunodeficiency virus (SIV), a close cousin of HIV, cause AIDS in
Asian macaques. In addition, chimeric viruses known as SHIVs, which
contain an SIV backbone with various HIV genes in place of the
corresponding SIV genes, cause AIDS in macaques. Further strengthening
the association of these viruses with AIDS, researchers have shown
that SIV/SHIVs isolated from animals with AIDS cause AIDS when
transmitted to uninfected animals (O'Neil et al. J Infect Dis
2000;182:1051; Aldrovandi et al. Nature 1993;363:732; Liska et al.
AIDS Res Hum Retroviruses 1999;15:445; Locher et al. Arch Pathol Lab
Med 1998;22:523; Hirsch et al. Virus Res 1994;32:183; Joag et al. J
Virol 1996;70:3189).
