Subject: The role of
antibiotics in the emmergence of AIDS
From: Study group AIDS therapy
felix.defries@bluewin.ch
To those affected,
their doctors and carers
To Media in developed and developping countries
Zürich, 15th June 2001
The role of antibiotics
in the emergence of AIDS
Dear Sir or Madam
From the enclosed articles
you may learn, what role the overuse of antibiotics plays in the
emergence of immune deficiencies and AIDS defining illnesses.
Chemical antibiotics (e.g.
sulphonamides, TMPSMX and Co-trimoxazole), that
have been repeatedly administrated from 1970 on in any kind of infections,
cause immunosuppression, resistant bacteries and toxic effects
like skin rash, nausea and vomiting, leukopenia, pancreatitis, hyperkalemia,
thrombo-cytopenia, toxic metabolites, elevated levels of liver
enzymes and methhaemoglobinemia. By destroying bacteria in the gut they
inhibit the production of immunoglobulins, needed for the body's inner
defences, and lay the body open to all sorts of bacterial, fungaland
viral infections, including those associated with AIDS. By their
strong oxydative effects they lead to a deficiency of
glutathionmolecules in cells, that is characteristic for the
development of AIDS defining
illnesses.
Patients showing this
immunodeficiencies induced by the overuse of this antibiotics
have been treated from 1985 on with nucleoside analog drugs (e.g.
AZT) designed for cancer therapy to induce program-med cell death.
By their cytotoxic effects
this substances destroy in the short run various
bacteria, fungy and viruses. In the longer run they damage CD-4 and
CD-8 helpercells, thereby inducing opportunistic infections such as cytomegalie,
toxoplasmosis, herpes simplex, PCP and hepatitis nonAnonB, con-sidered
to be characteristic for the AIDS syndrome. By the same effects
they damage the DNA in mitochondria resulting in severe irreversiable
damages in the brain, the muscles, the bone marrow and internal
organs.
Even after 1990 when this
effects of nucleoside analog drugs and chemo-antibiotics
were approved by animal trials, almost all patients with
AIDS defining illnesses and a positive result in HIV-antibody tests were
treated with this substances. Their immunodeficiencies and illnesses
were traced back to the HIV-retroviruses, which untill today have
not been approved to be transmittable viruses according to the established
rules in virology. From 1996 on nucleoside anlog drugs were adminstrated
together with synthetic protease inhibitors in AIDS patients.
As severe damaging effects occured also from this therapy the administration
of this cocktails was restricted in 2000 only to patients that
show full blown AIDS.
The promotors of the
HIV-AIDS-hypothesis, the producers of this substances
and the WHO now claim the broad administration of this immunotoxic
and cytotoxic substances in the developping countries. They still
don't want to investigate the real causes of AIDS defining illnesses
and the therapeutic means to restitute immunity in those affected.
Yours faithfully
Felix de Fries
Study group AIDS therapy
Geoffrey
Cannon: Superbugs, Nature's Revenge
Virgin Publishing Ltd.,
London 1995
Part Four: Apocalypse Now:
How Antibiotics Breed Disease
Chapter 15: Nature's Most
Malicious Trick?
Reasons to be careful -
Immunosuppression - a link with AIDS? - Increasing risk
of colon cancer.
Reasons to be careful
Once you know, that you
need the resident bacteria in your gut to protect
your health, and that antibiotics especially when overused may eventually
not only devaste these friendly flora but also may strip away the
outer immune defences in your gut, it is easy to see that prolonged course
of antibiotics can in time lay you open to all sorts of infections
and also non-infectious diseases.
Many diseases, some
serious, have evidently become more common in countries
like UK and the USA in the last 50 years. They may in part be caused
by medical treatment. Infants and children are vulnerable to repeated
ear, nose and throat infections. Girls and women are vulnerable to
repeated cysteitis and to fungal superinfection, which can become invasive. Antibiotics are
certainly one cause of this diseases and may be one cause of a variety
of bowel diseases and some forms of arthritis.
And the serious general
malaise known as chronic fatique syndrome may be in part a complication of
invasive fungal infection. Young children and old people are especially
at risk, as are the chronically ill. This in addition to the known
immediate or acurate ill-effects of antibiotics already described.
Once again, these are not
reasons to always avoid antibiotics. To repeat, they are a
precious resource: in case of reliably diagnosed serious invasive bacterial
infections their benefits far outweight their risks. But risks there
are: and many of the ill-effects of antibiotics are insidious, quite
likely not to be linked with the drug either by victims or their doctors.
Immunosuppression
Our resident gut flora
have another vital function not mentioned so far. They stimulate the
production of immunoglobulins, proteins in the blood integral to the body's
inner immune defences. Experiments show that animals with all their gut
flora removed, make only about one-fiftieth as much immunoglobuline as
normal animals. Commenting on this finding, the standard textbook
'Immunology' states: "If the commensal organisms of the gut are removed by
antibiotics, pathogenic organisms can readily gain a foothold", and
emphasises the importance of not disturbing the relationship between the
host and its indigenous flora.
Does this mean that
antibiotics are immunosuppressant drugs? This is an explosive question. Drugs
generally classified as immunosuppressants are very dangerous. They are
used only on people with cancer, and also after organ-transplants. They
greatly increase the risk of serious bacterial and viral infection, and
also of cancer, and are used only when patients are otherwise likely to
die.
In ordinary circumstances,
antibiotics are nothing like as dangerous as these drugs. As already
stated, one course of antibiotics destroys the bacteria in the gut but
not utterly, and a healthy balance of resident bacteria is usually
restored soon after antibiotic therapy.
The only class of
antibiotic that is commonly identified as immunosuppressive is
tetracycline, because of its profound destruction of so many species of
resident gut flora. And in a sense allergic reactions are reassuring
because as mentioned, they show, that the body's inner immune
defences are beeing irritated, and therefore obviously in working
order. Basically healthy people are very unlikely to disrupt their inner
immune defences by taking just one course of antibiotics.
Nevertheless, antibiotics
do have a suppressive effect on our defences against infection. Given
that our outer defences, including resident bacteria and the mucosal
lining of the body's inner passages, are an integral part of our
immune system, it follows inescapably that all antibiotics are by their
nature immunosuppressants -mildly so, no doubt, compared with the drugs
used on cancer and organtransplant patients, but immunosuppressive none the
less.
How much this matters
depends on the general state of the health of the individual, the type of
antibiotic and the strength and length of the course. As ever, babies
and little children, old people, hospital patients and anybody else
who is generally weak or ill are at greatest risk, and this includes
many, if not most people on the antibiotic treadmill, taking more and
more courses for recurrent infections.
Most vulneralbe of all are
people who are already immunosuppressed. But which came first;
immunosuppression or antibiotics?
Here ist the view of
Professor Sandy Raeburn, head of the departement of clinical genetics at
Nottingham University, a specialist in disease of young children. In 1972 he
wrote a paper for the Lancet, on "Antibiotics and
Immunodeficiency":
"Immunological-deficiency
syndromes were not observed before 1952. A possible explanation is
that some of these conditions are produced by administration of
antibiotics to certain individuals at a critical point in the development of
immune responses."
Dr Raeburn gave examples
of immunodeficiency diseases suffered mostly by babies and young children.
Combined immunodeficiency (DIC) lays infants open to
diarrhoea, thrush,
pneumonia and other infections, and may increase the chance of
cancer. Chronic granulomatous disease (CGD) also makes babies more
vulnerable to bacterial infections.
"This diseases were
not described before the antibiotic era" said Dr. Raeburn, "and the
usual view is that modern therapy has enabled affected patients to survive
longer. An alternative explanation, however, is that antibiotics have actually
led to immunodeficiency states - diseases which did not previously
exist".
He supports this proposal
by three lines of argument. First, since one of the main purposes of
the immune system (including the bacteria that have evolved with us) is
to protect the body against invading micro-organisms, 'removal
of bacteria by other means, such as rapidly effective antibacterial
therapy, could have profound effects - for example, in infancy, during
immunological development.' Later in life, antibiotics might provoke
bacteria, even the friendly flora, into producing poisons that the
immune system cannot handle. "The rarest clinical effects will
emerge sooner or later because antibiotics are so widely used".
Second - and here Dr.
Raeburn draws on his own clinical experience - while antibiotics work well for
previous healthy people with an acute infection, they usually
don't work for patients who are immunodeficient.
"Failures of
antibiotic therapy are often excused by an assumption that host resistance was
impaired. Could it be that infection persisted because the antibiotics
interfered with host resistance in a susceptible patient? I have seen
several patients whose infections progressed while they were receiving
seemingly appropriate antibiotics.
Third, he cited the
laboratory evidence showing that antibiotics make experimental animals more
vulnerable to infections by suppressing their immune responses
- some
very much more than others. Those at greatest risk of immunodeficiency
diseases caused by antibiotics will include: those born vulnerable; babies
and young children; people who are suffering from other diseases; and
anybody taking regular heavy doses of antibiotics. He concluded:
"If this theory is substantiated, it follows that antibiotics shoud be
reserved for life-threatening infections, until the risk of
immunotoxicity ist excluded in each patient".
I wrote to Dr. Raeburn
asking him if, in the twenty years since he had published thar Lancet
paper, he had changed his view. He wrote back saying:
"Since I
published that paper, there has been a vast amount of work on the interaction
between antibiotics and the immune system. Much of it bears my own
original hypothesis...
When a patient receives
antibiotic treatment, the beneficial effects due to antibacterial activity
could be reduced or even negated by deleterious effects on the
immune system". Overall, he said, antibiotics are beneficial, "but
in my special area of medical genetics, we might well see patients in which
the balance is set differently - for exaple in cystic fibrosis".
In 1984, a dozen years
after Dr. Raeburn's Lancet paper., Dr William Hauser of the Bosten
University Medical Center and Dr. Jack Remington of the Palo Alto Medical
Foundation, both specialists in infectious disease, published a
review of the scientific literature on the "Effect of Antimicrobial Agents on
the Immune Response" in the textbook Antimicrobial Therapy.
Antibiotics listed as having ill-effects on the human immune response
include: some aminoglycosides (gentamicin, tobramycin); a
cephalosoprin (cephalotin); chloramphenicol; a lincosamide
(clindamycin),
;various sulphonamides, and co-trimoxazole; various
tetracyclines;
sodium fusidate; and a number of anti-fungal and ant-tubercular drugs.
Penicillins are not included, and evidently do not have ill-effects on the
body's inner immune defences.
Hauser and Remington
comment:
There is clearly a need
for a better understanding of the potential
beneficial and deleterious
effects of antibiotic therapy on the host's immune
defences,
especially in the immunosuppressed patient.
Indeed there is. But when
antibiotics suppress our immune defences against disease, as
evidently they may do, then people given constant courses of antibiotics to
drive out infection will be not so much on a drug treadmill as caught
in vortex pulling them down deeper into disease.
Here is an appalling prospect. A child suffers middle-ear inflammation,
treated with antibiotics,
which then recurs because of antibiotics. A woman suffers cystitis,
which is cleared up with antibiotics, but which then recurs in a more
invasive form because of antibiotics. These infections occured in the
first place because of antibiotics taken in infancy and childhood.
Then people of all ages and both sexes suffer a cascade of diseases of the
gut, each stage accelerated by antibiotics, which eventually cause
irreversible infections carried by bacteria and by viruses that easily
break thrugh weakened immune defences. At some stage in this cascade, the
victims become chronically immunosuppressed, vulneralbe to invasion by
any infectious agent around...
The idea that medicine can
cure illness immediately and yet cause illness later may seem
strange. But in other areas of life we know that gain now can mean loss
later - this, after all, is one of the tenets of the Christian religion.
Or, to take two familiar analogies, we know we can drive to destinations
faster by breaking the speed limit, and we know we can spend our way
out of immediate trouble by running up and overdraft. We also know we
are running the risk of wrecking our car or our finances. A friendly
garage mechanic or bank manager will advise us to be careful.
A link with AIDS
When Professor Raeburn
wrote his paper, chronic fatigue syndrome was obscure, and AIDS was
unknown. When Drs Hauser and Remington wrote their review, neither disease
was common. While AIDS kills and CFS does not, the two diseases are in
some ways rather similar. Both are new, epidemic, afflict young
people, have no known cure, take many clinical forms and cause profound
debility. In the case of AIDS it is generally but not universally agreed
that the infectious agent ist the HIV retrovirus. In the case of
CFS there is a growing belief, that an enterovirus is involved.
As Professor James Mowbray
has said of CFS, why has the immunity of people who suffer AIDS
broken down? What is it that some people who are exposed to the disease
remain untouched while other become infected with HIV? Why is it that some
people who test HIV positive remain in good health for many years,
perhaps never suffering full blown AIDS, while others die rapidly?
Because AIDS is a new
disease, is deadly and is an accelerating epidemic with in 1990 alone an
estimated one million new cases of people worldwide infected with
the HIV virus, other sexually transmitted diseases seem less
important now. But at the end of 1990, the World Health Organisation
announced that more than 250 million new cases of sexually transmitted
diseases are reported every year. According to WHO Director-General Dr.
Hiroshi Nakajima, "they have reached epidemic proportion globally, and
if sexual behaviour is not modified and effectiv new prevention
programmes are not implemented immediately the resulting disease and
mortality rates will be even more staggering".
In 1990, 25 million new
cases of gonorrhoea and 3,5 million new cases of syphilis were reported
worldwide. Gonorrhoea is now often very resistant to penicillin, the
original durg of choice, in which case, treatment is either with massive doses
of penicillin, or other antibiotics including aminoglycosides,
sulphonamides or co-trimoxazole. Penicillin usually still works on
symphilis;
an alteernative drug is tetracycline. In the last half-century, other
sexually transmitted diseases have become more common. These include
genital ulcers, treated with sulphonamides ortetracyclines; chlamydia,
with tetracyclines, chancroid, with co-trimoxazole,
trichomoniasis, with metronidazole; and genital herpes, a viral disease.
More than any other
community, people whose lifestyle involves very many sexual partners are almost
certain to suffer combinations and permutations of
sexually transmitted diseases, which when bacterial are treated with constant
courses of antibiotics, often broad-spectrum and/or cocktails. Such
treatment over time provokes superinfection and drug-resistant superbugs
- so more antibiotics are used, often more toxic in their effect. On such a
drug treadmill, people who have constantly quenched their sexually
transmitted diseases with antimicrobial drugs are more vulneralbe to any
infection, whether bacterial, fungal or viral, and once infected, are
more likely to be overwhelmed.
In his book "The
Plague Maker, Dr. Jeffrey Fisher states that Dr. Luc Montagnier of the Pasteur
Institute in Paris, co-discoverer of HIV, believes that gross
overuse of antibiotics may be a co-factor with HIV development of full-blown
AIDS. This theory, sensation only because AIDS is the great deadly plague
of our time, is also believed by some homoeopaths. Can it be
true?
It makes microbiological
sense: there is some experimental evidence suggesting that
tetracycline has a side-effect of mutating mycoplasmas, including M. pirium and M.
fermetans, into virus-type micro-organisms that can invade
T-lymphocyte cells, whose function is crucial to the body's inner immunity
against infectious diseases. The Theory goes on to propose that if these
cells are also already invaded by HIV, the mutated mycoplasmas effectively
feed the HIV, activating them and enabling them to destroy T-lymphocyte
function, thus laying the victim open to a great range of infections
identified as full-blown AIDS.
On a separate point, Dr.
Fisher quotes other research scientists who confirm the findings of
Drs. Hauser and Remington, and who state that various antimicrobial
drugs, including sulphonamides, cephalosporins, antifungals and
antiparasitics are directly immunosuppressive in different ways and, when
overused, themselves increase vulnerability to infectious diseases.
If the mycoplasma theory
is true, it would follow that people who test positive for presence of
the HIV virus in their bodies, but whose lifestyles have not led
them to gross overuse of antibiotics, will be less likely to develop
full-blown AIDS. And indeed, haemophiliacs and others frequently show no
signs of illness for ten or fifteen years after
being accidentally
treated or transfused with clotting factors or blood infected with HIV.
If the mycoplasma theory
turns out not to be supported by evidence from other researchers, it
remains true that destruction of gut flora and damage to the body's
immunological defences by continual courses of antibiotics lays the body
open to all sorts of bacterial, fungal and viral infections,
including those most commonly associated with AIDS.
For men, the dream of
sexual liberation began in the 1940ies. American Gis believed that because
of penicillin they could go on the rampage with European and Asian
women during World War II, and then during the Korean and Vietnam wars,
without risk to themselves. The result is multi drug-resistant
gonorrhea.
But antibiotics retained their reputation as magic bullets throughout
the 1970s and 1980s, enabling increasingly wild lifestyles. In the USA
and other rich countries, this is the context of AIDS. It can be said, that
AIDS is a disease that was waiting to happen.
Comment in:
Clin Infect Dis. 1992
Dec;15(6):1066-8
Interactions and
toxicities of drugs used in patients with AIDS.
Lee BL, Safrin S.
Department of Medicine,
University of California, San Francisco.
As clinicians have come to
realize, patients who have AIDS are uniquely
predisposed to
drug-associated toxic effects and allergic reactions. In San
Francisco General
Hospital's first clinical trial involving patients with
pneumonia due to
Pneumocystis carinii, only one-third of all patients who were
treated initially with
either trimethoprim-sulfamethoxazole
or pentamidine were able to complete the
3-week course. Because of drug-related toxic
effects, most patients
required an alteration in therapy. In addition, with
the multi-drug approach to
management of infection due to human
immunodeficiency virus
(HIV) and its complications, drug-drug interactions
commonly complicate the
pharmacokinetics and toxicities of the
therapeutic agents used. Both factors
make caring for HIV-infected patients a complicated
and perplexing process for
the clinician. We've invited Drs. Belle Lee and
Sharon Safrin of the
University of California, San Francisco School of
Medicine to contribute the
AIDS Commentary this month.
Drs. Lee and Safrin are active investigators
in the field of pharmacokinetics and
conduct clinical trials of agents used in
the treatment of patients who have AIDS. In this
commentary, they review
what is known about the complexities involved in
treating patients with
AIDS and offer some practical suggestions for
management.
ACQUIRED IATROGENIC DEATH
SYNDROME (AIDS)
Pneumonias & Lung
Diseases
By Heinrich Kremer
Continuum Nov./Dec. 1996
PCP accounts for the
majority of Western AIDS diagnoses - yet the diagnosis of AIDS can
be given on the basis of a
presumptive diagnosis of PCP alone. A positive
"HIV"antibody test is not even
necessary. Is this definition alone creating a hothouse of fear and, with
its assumptions, distracting
patients and doctors from recognising the real processes of risk?
In particular, the
revelation that PCP is not an opportunistic infection challenges
itself the wisdom of drug
prophylaxis.
In 1996, the respected
British medical journal The Lancet began publishing a series of
special articles about HIV
and AIDS, addressing various aspects from vaccines to the
nervous system. All the
articles rashly assumed that an isolated retrovirus called HIV
causes AIDS.
In the following article,
Dr. Heinrich Kremer responds to one such article, by Dr. Miller,
on "HIV-associated
respiratory diseases". In a knowledgeable and inquisitive manner he
brings into unrelenting
focus the deeply disturbing way in which damaging medication has
helped create rather than
cure the problems of PCP and other conditions.
Pneumonia is a frightening
prospect for anyone, treating physicians included. Undoubtedly
prevention is better than
cure. But does this involves a fresh commitment to look behind
the plague-mongering to
the sensitivity of our biological systems, and the pressures of
present and cumulative
chemo-toxicity?
"Progress comes from
individual creation and imagination, not from the narrow dogmatism of a burgeoning
AIDS establishment."
-- The Lancet editorial,
July 6,1996
It was one of the early
pioneers of modern medicine, the German physician Rudolf
Virchow (1821-1902) who,
at the height of his career, said he wanted to become an MP in
order to see to the
completion of Berlin's antiquated sewage system, otherwise he could
not successfully fight
tuberculosis. How right he was! Only 100 years ago one worker in
three died of
tuberculosis. But until about 1950 tuberculosis had become rare in Western
industrial countries,
practically without recourse to drugs, which only became available
towards the end of the
1940s. Above all, improvements in hygiene, living conditions and
nutrition were
instrumental in curbing tuberculosis of the lung.
Nowadays, however, there
are modern successors to Virchow's causes of tuberculosis to
surprise us, namely,
"the association
between HIV infection and tuberculosis is well described ...
Tuberculosis in an
HIV-infected individual is an AIDS-defining illness ..."
This claim is one of the
many assertions by Dr. Miller in his article
"HIV-associated respiratory
diseases," which he divides into eight infectious and four non-infectious
diseases:
Infectious:
1)
Upper respiratory tract infections,
2) Acute bronchitis,
3) Acute sinusitis,
4) Bacterial
pneumonia,
5) Pneumocystis carinii pneumonia,
6)
Mycobacterium tuberculosis,
7)
Mycobacterium avium intracellulare,
8) Fungal pneumonia;
Non-infectious:
1)
Kaposi's sarcoma,
2) Lymphoma,
3) Non-specific interstitial pneumonitis,
4) Lymphoid
interstitial pneumonitis.
Now, it turns out to be
something of an advantage for me as a medical doctor to have
kept away from conferences and
not to have much beyond schoolboy English, because I had to
check up on the exact
meaning of 'association' and 'associated' in the Oxford Dictionary, to
find that they mean
'connection in the mind' - in other words, we are dealing with a
suggested mental, rather
than causal, connection between HIV and respiratory disease, as
well as between HIV and
tuberculosis. Does Dr. Miller want to lecture us on ideology
rather than biology? Not
at all, Dr. Miller quickly explains:
"tuberculosis is a
potent stimulator of cell-mediated immunity, activating HIV
production in lymphocytes
and monocytes/macrophages latently infected with
HIV, which brings out the
spread of HIV infection to other cells."
It dawns on me why
tuberculosis -1.7 billion infected worldwide, 600 million cases
annually, 2 million
deaths, of which 95% are in developing countries; in Western
countries less than 0.05% of the
population is affected by the disease, of which more than 95% are
homeless, alcoholics,
IV-drug users, asylum seekers - "is an AIDS-defining
illness". Up till now AIDS-defining
illnesses were supposed to be the consequence of alleged
causative HIV infection.
It now seems that diseases which first have to rouse
"dormant HIV" from CD4
lymphocytes and macrophages are also part of the AIDS collection.
This means every disease
process which has in any way reacted with thymus-matured
immune cells (T-cells) can henceforth be renamed an "AIDS-defining
disease", if it can simultaneously be
"associated with HIV." There are no limits, therefore, to what can be
done in the virtual,
toytown world of AIDS, since in practically all serious diseases there
is some contribution of
cellmediated immunity. Dr. Miller grabs this opportunity by the
throat and lists all
"11 IV-associated respiratory diseases," and observes that "the
clinical features of upper
respiratory tract infections, acute bronchitis and acute sinusitis are
the same in HIV-infected
individuals as in those without HIV, but their frequency is
increased."
So saying, Dr. Miller has
deftly dealt with three of his eight "infectious
HIV-associated respiratory
diseases."
Bacterial Pneumonias
But it gets more serious
when Dr. Miller classifies as the fourth HIV-associated disease
group "bacterial
pneumonia".
"The spectrum of
bacterial pathogens is similar to that of community-acquired
pneumonia in the
non-HIV-infected population."
In this disease group,
too, Dr. Miller offers an intellectual prop to the
"HIV-association":
"bacterial pneumonia
occurs more frequently in HIV-infected individuals than in
the general population and
is especially common in HIV-infected intravenous
drug users."
Indeed, in the general
population in Germany, for example, less than 1% of the population
is affected by bacterial
pneumonias. IV-drug users suffered more frequently from bacterial
pneumonias long before
AIDS came along for reasons well known to the venerable
Virchow - unsatisfactory
hygiene, malnutrition, bad housing etc., etc. (see above). The
really important point,
however, Dr. Miller conceals from us: IV-drug users classified
as "HIV-infected"
suffered from bacterial pneumonias, as a comprehensive study in
Berlin has shown, whereas
non-bacterial pneumocystis carinii pneumonia (PCP) the most
frequent "HIV
associated respiratory disease" in Miller's list (and the most frequent
"HIV associated disease"
or "AIDS-defining illness" altogether in the West) does not to all
intents and purposes
feature at all in IV-drug users who are not homosexual.
We can now see more
clearly why bacterial pneumonias that are on the official list of
AIDS-indicator diseases in
adults only if they occur more than twice a year, have to be
wangled in under the guise
of 'HIV-associated.' Without the creation of
"HIV" no-one would ever have dreamt of
the need to diagnose IV-drug users as "AIDS," because
PCP and Kaposi's sarcoma, the
most common "AIDS indicator diseases", do not occur in
non-homosexual IV-drug
users in Western countries despite a laboratory finding of
'HIV-positive.'
Why does Dr. Miller
conceal these facts in his Lancet article? Dr. Miller lumps together
everything which in
patients labeled "HIV positive" could be called respiratory tract
diseases. Because the
introduction of a new cause for these long-known diseases from
the same long-known causes, in
the very same long-known categories of persons, would seem
rather untrustworthy, he
makes these 'old-timers' among the common respiratory tract
diseases the driving force
of the newly invented "HIV" infection and lumps them together
as "HIV-associated
disease" or "AIDS related processes" as he likes to call them. That
these patients are thereby
exposed to an increasing number of pharmaceutical drugs does
not seem to worry Dr.
Miller unduly, as his treatment of PCP, the fifth of the eight
"HIV-associated"
diseases in his list shows.
Pneumocystis Carinii
Pneumonia
Strangely, pneumocystis
carinii pneumonia turns up here as a "genuine"
AIDS-indicator disease under the
conditional heading of "HIV-associated respiratory disease."
Has Dr. Miller lost faith in the
orthodox belief in "AIDS"? Not at all. He quickly goes on to
explain:
"P. carinii remains a
common respiratory pathogen in individuals with
AIDS."
Miller again uses the
idiosyncratic phrase "in individuals with AIDS." A doctor's
diagnosis of PCP alone is
entirely sufficient according to the most official AIDS definition
to say "this patient
is an AIDS case" or "this patient has AIDS."
And this attribution of "AIDS" due to
the diagnosis of PCP alone, establishes 40% of all clinical "AIDS
cases" and about 80% of all
"AIDS deaths" in Western countries.
The official definition of
the authoritative American CDC has since 1987 remained
unchanged - an AIDS
diagnosis is justified even if only a presumptive diagnosis of
PCP exists, and in the absence
of any laboratory suggestion of "HIV-positivity,"
and without any noticeable decline of
immune cell values in blood serum.
Thus, PCP was from the beginning
synonymous with AIDS, even without the 'S' (for
Syndrome, of another 28
diseases) and without the 'ID' (for immune-deficiency,
interpreted from decrease in CD4
lymphocytes in the bloodstream), and without the 'A' (for Acquired
"HIV
infection"). Naked PCP therefore is the seed of "AIDS".
Everything else Dr. Miller
and his colleagues
associated, as "connections in the mind".
In plain language, if
there are other good reasons for the occurrence of PCP in
homosexual patients, the
"HIV-associated diseases" just melt away as yesterday's snow.
In this respect Dr. Miller
comes up with a genuine surprise. Miller explains in
considerable detail that
according to the latest research findings, the pathogen responsible
for PCP is an airborne
fungus and not, as thought up till now by AIDS doctors, a
unicellular animal
parasite. This implies an enormous difference from the diagnostic and
therapeutic point of view:
and in the real case of an individual patient, this
reclassification can mean the difference
between forecasting life and death. Until now epidemiologists
assumed PCP was a case of zoonosis,
ie. a ubiquitous animal, prevented by cell-mediated
immunity from breaking
through the body's immune barrier and causing devastating
pneumonias. This
assumption was seemingly based, according to Dr. Miller, on the finding
that 90% of children and
adults in Western countries had antibodies to P. carinii without
contracting that form of
pneumonia. But now it turns out the essential assumption -
that the presence of antibodies
indicates the presence of the pathogen - was fundamentally
mistaken:
"P. carinii cannot be
detected with DNA amplification or monoclonal
antibodies in
bronchoalveolar ravage fluid or necropsy lung tissue of
immunocompetent
individuals and low levels of P. carinii are detected in the
lungs of only 20% of
immunosuppressed HIV-positive patients with respiratory
episodes and diagnoses
other than P. carinii pneumonia."
The conclusion is,
therefore, that "HIV" was invented in order to explain the apparent fact
that CD4 lymphocytes in
ostensibly 'hitherto healthy' individuals could suddenly no longer
hold in check the
pneumocystis protozoa which had been there all along. The simple
explanation which the now
shattered HIV/AIDS theory led to, was: "HIV" is
transmitted in semen, blood and blood
products to the recipient, "HIV" destroys the thymus matured CD4
lymphocytes, the
pneumocystis protozoa escaped their dead guards and kill their up till
then healthy host.
"HIV" was invented in order to explain the apparent fact that CD4
lymphocytes in ostensibly
'hitherto healthy' individuals could suddenly no longer hold in
check the pneumocystis
protozoa which had been there all along.
According to this nightmare scenario anyone
with "HIV" in his CD4 cells dies.
But suddenly now,
everything turns out to be completely different:
Pneumocystis protozoa
cannot escape from the CD4 immune cells, because pneumocystis
protozoa are not there.
Instead, since P. carinii is a fungus, is not transmitted in semen
or blood, and is passed on
through the air. This fungus, as Miller informs us, can be
disposed of easily in 80% of
"immune-suppressed HIV positive patients with respiratory episodes
and diagnoses other than
P. carinii pneumonia," without leaving a trace, and leaving in the
rest of these
"immune-suppressed HIV-positive patients" just "low levels" of P. carinii
(whatever that may mean).
So, what has the
laboratory finding of "HIV-positive" got to do with P. carinii pneumonia?
What conclusions does
Miller draw from his newly discovered findings? Answer: none.
Miller simply reports the
fact and carries on treating his patients as before:
"The regimen of first
choice for primary and secondary prophylaxis of P. carinii
pneumonia is co-trimoxazole, 960 mg once a day or three times a
week.... For treatment, first choice is
high dose co-trimoxazole (100 mg/kg per day of
sulphamethoxazole and 20
mg/kg per day of trimethoprim) in two or four
divided doses, orally or
intravenously, for 21 days."
The important point arises
- how does the metabolism of a unicellular animal
(protozoon) which normally just
vegetates as a harmless opportunist in the undamaged environment of a
lung differ from the
metabolism of a unicellular fungus - an external "recycling
specialist"
- which, even in
"immune-suppressed patients" apparently thrives only when suitable
growth conditions are
present in the lung? Miller, unsurprisingly, is silent on that
question.
Another question is who or
what is responsible for the substrate, the suitable growth
conditions, for P. carinii
in the lung? "HIV"? The patient? Or his treating doctors?
The imaginary retrovirus
"HIV" or a shortage of CD4 cells (allegedly massacred by
"HIV") cannot be
decisive for creating the special environment in the lung which enables
P. carinii to multiply
freely. Miller himself observes that:
"many
immunosuppressed HIV-positive patients do not have in the lung any P.
carinii or show only
traces of it."
The question arises,
therefore, whether cell-mediated immune deficiency, the laboratory
finding of
"HIV-positive", and the production of the substrate for P. carinii could not all
be traced back to a
systemic change in the body's metabolism.
Miller provides an important clue by
mentioning that administration of corticosteroids to rats can provoke
PCP. Experiments of this
kind date back to the 1950s which Miller does not mention, after
what was later called PCP
was first recognised in the 1930s in premature babies. Similar
symptoms of atypical
non-bacterial pneumonia (as opposed to typical bacterial
pneumonia) were diagnosed
in the 1940s in children and adults in famine conditions. So,
what do the
steroid-treated rats, the premature babies and the starving children after
the Second World War have in
common? (Note: PCP was at the time practically unknown in
the United States).
The premature babies
hardly stood a chance before modern treatments came along. They
suffered from their
immature lung cells a highly acute oxidative stress which in turn led
to massive hypercortisolism.
They mostly died from bacterial infections. These could be
controlled more
successfully after the introduction of the first broad-spectrum
sulphonamide, prontosil,
at the end of the 1930s. But then they died instead from PCP.
Although the sulphonamide,
which is a folic acid antagonist, [i.e. prevents the building of
folic acid] successfully
halted the production of bacterial proteins and hence
bacterial reproduction itself, at
the same time they raised the catabolic stress [see footnote].
Because the necessary
maturation of CD4 lymphocytes (T-cells) in the thymus gland is
very susceptible to
hypercortisolism and systemic oxidative stress, the task of
T-lymphocytes to dispose
of the extremely increased turnover of cells became practically
impossible: and the
resulting decomposition products of the catabolic metabolism
especially in the lungs
which are particularly susceptible to oxidative stress, built
the special conditions for the
ubiquitous airborne spores of P. carinii to thrive in.
These rather complex patho-physiological processes (unknown
about, of course, in the 1930s) would also explain
the PCP seen in rats which had been treated with
corticosteroids while
under antibiotic treatment.
Hypercortisolism induces a
characteristic 'famine metabolism' which leads to complicated
systemic changes in growth
and decay of the body at the molecular level, and provides the
substrate for the highly
specialised Pneumocystis fungi to grow on.
If this vital emergency
condition, under constant stress factors becomes a fixed lasting
condition, as in the
starving children of post-war Europe or in parts of Africa today,
thymus-dependent cells
(T-cells) decrease. In the normal course of events these T-cells
have to get rid of 1012
spent body cells a day: by halting the maturation of T-cells the
table becomes richly set
for P. carinii and other microbes to thrive. These unwelcome
scroungers can only be
chased away from this paradise of theirs, by abolishing the fixed
emergency conditions that
created it. This explanation is confirmed by the animal
experiments quoted by Dr.
Miller - 75% of P. carinii were found to have been disposed of
within one year of ending
the artificially induced hypercortisolism.
So, what could Dr. Miller
have learned from this brief glance into the history of PCP to
benefit his patients,
ostensibly stricken with "HIV-associated respiratory
diseases"? First, that PCP and the fungal
pneumonias could thrive very happily before AIDS came along -
and long before any
hypothesised retrovirus (which is not supposed to have existed before
1978) could have been
involved - under the systemic environmental changes in the lung
due to excessive
situations of oxidative stress under a persistent catabolic level of
metabolism.
Secondly, Dr. Miller could
have learned that the common factor between the phenomena
called "CD4 cell
immunodeficiency", P. carinii growth conditions, and the laboratory
finding of "HIV
positive" can be found in the fact of excessive forced oxidative stress.
The construction rules of
the "anti-HIV antibody test" lead also to this conclusion. Dr.
Gallo and his colleagues
brewed their test soup from already overstimulated CD4
lymphocytes obtained
mainly from the serum of PCP patients as well as from cells of a
particularly
division-prone leukaemia cell line, spiced this with powerful oxidising
agents, called mitogens,
added a generous dash of hydrocortisone, and incubated it
thoroughly. They then
fished out of this brew a mixture of proteins which they ascribed to a
hypothetical retrovirus,
HIV. It follows that these proteins (antigens), released under
the oxidative stress in the
test-tube, will necessarily bind to their complementary proteins
(antibodies) from the
serum of patients who had themselves, due to pathophysiological
processes, formed proteins
analogous to the test antigens from Gallo's brew. Antibodies
found in HIV-positives are
therefore to be seen as nothing other than increased levels of
auto-antibodies against
endogenous proteins which have been produced as a result of
highly increased
cell-turnover under chronic oxidative stress.
Thirdly, Dr. Miller could
have learned from all these findings that these laboratory
artefacts known as
"HIV-positives", represent anything but the presence of a
transmissible mass epidemic due to semen
and blood.
The annual incidence of
the false diagnosis "HIV-associated diseases" for the
whole population of Germany is
0.002%. This result contradicts eloquently the absurd
apocalyptic predictions of
AIDS doctors. The official annual rate of new infections in the
general population in
Germany of the clinical misdiagnosis "HIV associated P. carinii
pneumonia" is
practically 0.00%, and among gays amounts to just about 0.05%. This true
rate, differing starkly
from the predicted rate, is well within the range of other
epidemiological burdens of
other population groups, ea. the annual incidence of lung
cancer in all smokers is
0.1%. On the other hand, the annual rate of miscarriages due to
folic acid shortage in
mothers is also around 0.1% (and is strikingly close to the
incidence of folic acid inhibition
following medication with co-trimoxazole, of which more below.)
Medical Treatment
Perhaps the most important
lesson for survival of those affected is the question: what is the
effect of the medical
treatment on the development and course of "HIV-associated"
P. carinii pneumonia.
Dr. Miller is quite
revealing in two respects of this without seemingly being aware of
the consequences this entails.
First, he is perplexed:
"despite the
widespread introduction of effective primary and secondary
prophylaxis, P. carinii
pneumonia remains a common respiratory pathogen in
individuals with AIDS and
continues to account for almost half of all respiratory
episodes."
Without in any way
justifying the alleged efficacy of his primary and secondary
prophylaxis, he defines
his preferred mixture of co-trimoxazole with seemingly precise
milligram amounts as a
multipurpose-weapon prophylaxis against prokaryotic and
eukaryotic unicellular
life forms in three domains of life at the same time: against fungi
(including P. carinii
pneumonia), protozoa (including toxoplasmosis gondii) and
"bacterial
infections."
"The regimen of first
choice for primary and secondary prophylaxis of P. carinii
pneumonia is co-trimoxazole 960 mg once a day or three times a
week; this may also afford some
protection against bacterial infections and against reactivation
of cerebral toxoplasmosis.
"
The curious reader also
gets to learn from Dr. Miller, 15 years after being first reported
by the CDC (June 1981) about
the failure of treating homosexuals with co-trimoxazole who
had PCP (two out of five
died), but nothing of the mechanism of this chemotherapeutic
agent (often wrongly
prescribed as an 'antibiotic').
Co-trimoxazole (better
known under its trade names Bactrim and Septrin) contains a
combination of
sulphamethoxazole, a sulphonamide, and trimethoprim, a cytostatic agent
which is also used to
treat leukaemia in the same form, ie. to destroy white blood cells!
Sulphamethoxazole inhibits
the synthesis of folic acid which is essential to life, by
substituting the
pare-amino-benzene (PABA) moiety, so that the enzyme responsible for
folic acid synthesis is
consequently blocked.
Trimethoprim inhibits
conversion of folic acid into the biologically active form
of tetrahydrofolate by
blocking the enzyme dihydrofolate reductase. Without
tetrahydrofolate, essential precursors for
new DNA cannot be synthesised. For example, the nucleoside
uridine has to be
methylated by methylentetrahydrofolate to form the essential DNA
building block, thymidine
triphosphate (TTP). This is the same component that is
displaced with the
notorious cell poison, azido-thymidine, better known as AZT,
Zidovudine or Retrovir.
Co-trimaxazole, therefore, works in a different way, but with a
similar result to AZT, as
a DNA blocker!
The consequences of
inhibiting essential metabolic pathways for growth, cell
differentiation and
division are fatal. The synthesis of essential nucleic acids, proteins
and enzymes develops faultily,
or ends completely.
Cell Damage
This treatment with
combined trimethoprim/sulphamethoxazole (=co-trimoxazole) is
especially serious for the
functioning and fine structure of mitochondria in nucleated
(eukaryotic) unicellular
and multicellular species (protozoa, fungi, plants, animals,
humans). Mitochondria -
so-called organelles - are the major suppliers of energy in
human cells (except in red blood
cells). They are endosymbionts (former bacteria with a double
membrane). They contain
remnants of their ancestral genome. This mitochondrial DNA
(mtDNA) is irreplaceable
in the synthesis of protein sub-components of the respiratory
chain. For respiration,
activated electrons in the respiratory chain from nutrients using
oxygen are built into the
universal energy source for the entire cell, adenosine
triphosphate (ATP). If the synthesis of
precursors of DNA is harmed through chronic or high dose treatment
with co-trimoxazole the
mitochondrial DNA is damaged and altered which in consequence
impairs mitochondrial
proteins, as well as the proteins of the respiratory chain, and ATP
production therefore
decreases. This leads to increased oxidative stress and to an increase
in toxic oxygen free
radicals. A vicious circle is set up once the ATP levels reach a
critical low, and if the
special molecules which normally remove harmful oxygen
intermediaries are all
used up, then further DNA damage arises. The cell initiates
programmed cell death,
because the ion pumps which regulate the balance of the flow of
manifold molecules of
building supplies and working materials into and out of the cell
necessary to maintain cell
function, fail for lack of fuel in the form of ATP.
Incidentally, DNA blockers
such as co-trimoxazole and AZT, fundamentally damage
predominantly the
mitochondrial DNA, because the mitochondria cannot repair any
mismatches or breaks in
their DNA unlike the much longer and specially protected
double-stranded DNA in the
cell nucleus which can. DNA in the nucleus is passed on by
sexual reproduction and is
recombined, whereas mitochondrial DNA is propagated
asexually through the
maternal egg cell, which means that mutation errors are not corrected
but conserved. The
mutation rate of mitochondrial DNA is 5-10 times higher than for
nuclear DNA. The nuclear
DNA, being surrounded by its own membrane is physically
better shielded, as well
as benefiting from protective proteins and enzymes from any
damaging effects of the
metabolism than is mitochondrial DNA, which in bacteria is
scattered loose throughout
the cell plasma, and in several copies.
The above basic facts of
cell biology apply, of course, with greatest force in rapidly
maturing cells with short
half-lives, especially the thymus-matured lymphocytes (T-cells),
whose job is not only to
recognise and, with the help of other immune cells eliminate,
foreign proteins, but also
to remove altered selfproteins without causing inflammation. If
this cannot be done
adequately because of infectious, toxic, nutritional, psychological
or other overload, the body
enters a state of emergency: the B-cell system is stimulated to
produce antibodies and
autoantibodies as well as macrophages and many inflammatory
mediators and the entire
metabolism is transformed. Over the short term, the body can deal
with such a state of
emergency. If this state persists, however, a chronic maturation deficit
of T-lymphocytes (T-helper
cell deficiency) arises, and the now permanently changed
environment becomes the
feeding ground (substrate) for the recycling activity of
fungal parasites (in Greek,
parasite means unwelcome scrounger) and as a consequence of B-cell
activation, specific
autoantibody profiles make the "anti-HIV antibody test" turn
positive, just as in some autoimmune
diseases such as rheumatoid arthritis and lupus
erythematosus.
Under these conditions of
highly acute state of emergency such as is found in
"immune-suppressed
patients," it does not require the wisdom of Solomon to see that the
treatment methods of Dr.
Miller and his colleagues will induce precisely that which they
seek to avoid, namely, an
Acquired Immune Deficiency Syndrome (AIDS) induced through
wrong medical practice.
Why does Miller apparently
not know anything of the special vulnerability of
mitochondria to co-trimaxazole? Does he
not know that in wanting to stop fungi, protozoa and bacteria
prophylactically, he
simultaneously attacks the driving force of all body cells, the
mitochondria. as well.
since they are former bacteria themselves?
Dr. Miller comments
truefully: "as many as 25% of
patients receiving prophylactic co-trimoxazole develop
adverse drug reactions ...
50% of patients receiving treatment doses likewise
develop adverse
reactions."
But Dr. Miller describes
only the massive "side-effects" of short term therapy, though he
appears to be genuinely
surprised by their intensity in "HIV-associated
diseases." "There is no clear
explanation for such a pronounced increase in adverse
reactions to co-trimoxazole which is about 20% greater than
seen in the general population."
It is a pity that he does
not give some thought to the long-term use in prophylaxis of
folic acid inhibitors like co-trimoxazole (let alone in combination with
AZT (zidovudine), ddC (zalcitabine) ddI (didanosine), D4T
(stavudine), 3TC (2'-deoxy-3'-thiacytidine),
the newer protease inhibitors (saquinavir,
ritonavir, indinavir, neltinavir) or the newest
non-nucleoside reverse
transcriptase inhibitors (delavidine, nevirapine and others.)
Are not the long-term
damaging effects of using combined folic acid inhibitors really the
major cause and not the
consequence of what Dr. Miller and colleagues perceive to be
"HIV associated
disease?"
Drug History
Co-trimoxazole was brought
into clinical use in the early 1970s, ie. more than 20 years
ago. Individually,
sulphamethoxazole and trimethoprim inhibited the growth of pathogens
only, whereas both
together as co-trimoxazole killed off a wide range of microbes.
This was of great
significance in the treatment of multiple infections of a minority
of homosexuals in the large
Western metropols. The purpose of treatment in most cases
was simply to suppress as
quickly as possible the wide spectrum of microbial growth
encountered. Co-trimoxazole quickly became the wonder drug with
specialist doctors and their homosexual patients
in Western metropols; this double-action folic acid inhibitor was
used not only to treat but
to forestall (incredibly, often by selfadministration),
unthinkingly, in exactly the same way as
nowadays Dr. Miller and his colleagues do, too - moreover, in
far too high doses and for
far too long a time - especially against the often refractory
urinary tract and
intestinal infections, and atypical pneumonias in this group of patients.
A literature search since
1970 does not come up with a single publication about the
"side-effects"
of co-trimoxazole on the functioning and fine structure of mitochondria,
nor on the connection between
T-cell deficiency itself and co-trimoxazole; yet there
has always been ample evidence
in the literature for the damage caused to all white blood
cells (including
lymphocytes) in various groups of patients, even during short-term use of
co-trimoxazole! The only
investigation of up to 45 days after beginning treatment with
co-trimoxazole was
conducted in Britain by the General Practice Research Group in
1988-93. Since folic acid
reserves in man can last up to 4-5 months, significant damage
to patients with
"HIV-associated infectious diseases" often manifests itself only after
long-term prophylactic use
exceeding eight weeks, which is then interpreted as AIDS
symptoms.
Surprisingly, until the
appearance of AIDS in 1981 there were no reports in the medical or
pharmaceutical press about
the damaging effects of co-trimoxazole use amongst
homosexuals, although the
"side effects" in this group should have stood out like a sore
thumb, because of the high
dosages and duration of treatment. The matter was obviously
declared a taboo subject
until P. carinii fungi as a recycling agent began to run amok in
the lungs of these patients,
sometimes after they could not be controlled even with high
doses of co-trimoxazole (as was
first reported by the CDC as long ago as June 1981).
Instead of at least by
then asking themselves what the damaging consequences of
chemotherapy in this group
might be, all those concerned indulged in a fit of collective
mental repression
regarding the interpretation of the symptoms they were witnessing,
which later on became
rationalised as a "new lethal syndrome due to a new pathogen."
Egged on by a prurient
media relishing plague fantasies, the medical establishment
transformed a set of new
and old symptoms into an apparently uniform disease process
using the codes
"AIDS-related processes" and "HIV-associated diseases" which
supposedly resulted as a
wide chain-reaction of the primary effect, a virus invasion, which
anyone could catch through
sex and blood.
This interpretation had
the tremendous advantage over more mundane explanations that
neither the doctor nor the
patient had to question their own role in the dynamic of the case
history; the new syndrome
started, so to speak, a-historically. The pharmaceutical industry
could exploit the ensuing
fear of death with impunity, instead of initiating a fundamental
reappraisal of
unphysiological chemotherapy and treatment, involving the testing and
use of ever more powerful
combinations of highly toxic mixtures on a global scale, financed
by all of us, in a
seemingly heroic battle against a "plague threatening
humankind."
The world's largest
manufacturer of co-trimoxazole has meanwhile confirmed in writing
that there have never been
any investigations into the effect of folic acid antagonists on
mitochondrial integrity.
Strangely enough though, the indications (recommended
circumstances under which
to prescribe a drug) at least in Britain and America for
co-trimoxazole, have been
severely reduced, because of frequent side effects during short
term use (cf. BNF, FDA
guidelines). Excepted from this change: special indications of
prophylactic and
therapeutic high doses and longterm use and in frequent intermittent
therapy (itself a
long-term use because of cumulative damage) were expressly permitted
for
"HIV-infected" patients and "PWAs".
In this light, the
concerned statement of Dr. Miller: "despite the
widespread introduction of effective primary and secondary
prophylaxis, P. carinii
pneumonia remains a common respiratory pathogen in
individuals with
AIDS" becomes a self-fulfilling
prophecy.
In the early 1980s the use
of co-trimoxazole had reached the very high annual incidence of
5% of the population,
about equal to that of alcoholism, while use of
co-trimoxazole by homosexuals in Western
countries (the taboo subject), in particular in metropols and in the
neighbourhoods of
specialised practices and clinics must have likely been, and continue
to be, considerably higher.
It was recommended to restrict the general indication of the drug,
because of the high level
of damage to blood cells, (including lymphocytes) while,
gruesome to relate, the
prophylactic and therapeutic indication for already
immune-suppressed
patients, stigmatised as "HIV infected" and "PWAs", were
relaxed.
If the number of CD4 cells
necessarily declines because of DNA blockage and
mitochondrial damage
through co-trimoxazole (because of increased cell death and
inhibition of maturation)
then "AIDS" will be diagnosed, and the range of DNA blockers
and mitochondria killers
constantly enlarged. The blind zeal of virus hunters leads them
to use ever more frantic
chemistry without, as Dr. Miller shows, ever stopping to think about
the vital basic conditions
of the intertwined biospheres of our bodies. The patient will
go through all the stages of
AIDS described in textbooks, and at the end of it, all the
participants will feel
bitter at having lost the battle, at great sacrifice against a fickle
enemy, despite calling on
all means available; the patient will have dutifully suffered a
ritual death for the sake
of a plague-hungry society; the frustration of the doctors
and their companions in death will
have been transformed into aggression against those who have
insisted all along on a
genuine re-evaluation of their actions.
Pre-existing Immune
Deficiency
If the premise of an
inexplicable immune deficiency affecting hitherto completely
healthy individuals had turned out
to be true, then the virus-AIDS theory could have been a
reasonable working
hypothesis. But because AIDS (according to the official CDC
explanation) is supposed
to be a serious disease of acquired immune deficiency without
pre-existing or induced
immune deficiency, it has to be stated quite unequivocally that
such AIDS cases have never been
found up till now, except in the form of a medical mantra of
plague propaganda, because
in all verifiable cases, demonstrable immune-suppressive
disease and/or treatment
have always preceded them.
There has never been a
need, therefore, to explain an inexplicable immune deficiency,
because the causes were
there for all to see. And a new virus was entirely redundant for an
understanding of the
disease process, irrespective of whether the suggested retrovirus HIV
existed or not. For
example, the annual incidence in Germany of AIDS in the population as
a whole is just 0.002%,
and amongst homosexuals 0.1%. Intriguingly, more than 60% of
all "AIDS-cases"
in a population of 80 million occur in the immediate vicinity of six
large university clinics in six
towns, which rather supports the view that AIDS should be called
an "Acquired
Iatrogenic Death Syndrome."
Furthermore, according to
Dr. Jager (in a live interview), one of the leading German
AIDS-authorities,
(President of the Curatorium for Immunodeficiency, Munich)
in the period from the ostensible
beginning in 1981 to 1996, there has not been a single case of
male or female HIV
infection in the age group 14-20 (not even in homosexuals!), although
every school kid has had
the exact opposite drummed into him, which is proof that the
advocates of HIV/AIDS are
by now unwilling to separate fact from fiction, even for the
sake of the patients
entrusted to their care.
Plague Mania
Dr. Miller really should
have another look at Virchow's writings in order to understand
why TB had practically
lost all its horrors in Western Europe without use of
chemotherapy, and why now,
in his own words: "multiple drug
resistant (MDR) tuberculosis has emerged as an important
clinical problem in
HIV-infected patients in the USA." Dr. Miller fails to
mention, however, that chemotherapy for mycobacterium tuberculosis
and mycobacterium avium
intracellulare (No's 6 & 7 in his list of "HIV-associated
infectious diseases")
also require high levels of folic acid, thereby inducing a
relative shortage of folic acid,
ideal conditions for DNA mutation to occur.
In Africa by the way, in
a different mycobacterial
disease, leprosy, the anti-HIV antibody test reacts positive as
well. Because African AIDS
(apparently 90% of all AIDS cases world-wide) is as a rule
nothing other than old
well-known clinical conditions such as TB, malaria, hepatitis,
diseases caused by worms
and 'slim', (all the result of poverty, hunger and inadequate
hygiene, in the sense that
Virchow meant), there the "HIV associated respiratory
tuberculosis" in Dr.
Miller's terminology, turns
