If you are willing to believe the medical as well as the general press,
the world today is again and again beset by new big epidemics. First AIDS,
then hepatitis C, now BSE. These new plagues differ from the plagues of
the past in one respect: The number of affected people is relatively small.
While the old plagues annihilated whole towns, the number of people who
actually fall ill with the "new big plagues" is very low. In
the case of AIDS there are about 2000 "new infections" (HIV
antibody positive) every year, and 600 deaths [in Germany]. Hepatitis
C hasnt led to a significant increase of liver cirrhosis, and regarding
BSE, we still dont have even one clinical case in our country, while
the press has been talking about BSE crisis or epidemics for weeks.
The epidemic-like character of these diseases is generated by a molecular
biological phenomenon, namely so-called test explosions. Today molecular
biology is capable of detecting the smallest quantities of DNA or RNA
with the PCR (Polymerase Chain Reaction) and able to produce antibodies
against it. The connection between what has been isolated in humans or
animals, and the presence of clinical symptoms, is a mere hypothesis.
This is perfectly illustrated in BSE, where a testing epidemic has also
taken place now, and still not one clinical symptom (a mad cow) has appeared
Because the symptoms are often missing, they must proclaim endless latency
periods, up to 55 years (between infection with the "BSE pathogen"
and developing the new variant of Creutzfeld-Jakob-Disease). But lets
start with AIDS, the first of the big new plagues.
AIDS manifested itself in the early 80s in San Francisco and affected
only homosexuals, who at the age of [about] 30 developed PCP (Pneumocystis
Carinii Pneumonia) and in part died of it. These first patients, whose
cases were published by Dr. Gottlieb, had two things in common; they were
homosexual and they were heavy drug addicts (cocaine, amphetamines, Amyl
Amyl nitrite is a sex drug, that is almost exclusively used in homosexual
community and which is induced in large quantities via inhalation. Nitrates
are, testable in animal research and in lymphocyte cultures, immuno-toxic
and cytotoxic as well as cancerogen (Source: NIDA, National Institute
of Drug abuse). Before the acronym "AIDS" was born, the same
thing had the name GRID (Gay Related Immune-Deficiency). During the first
years science assumed a lifestyle disease, because it was obvious that
AIDS only occurred in certain communities (homosexuals who lived the "fast-lane-lifestyle").
In 1983 the US health minister proclaimed on a press conference that a
US researcher had discovered a retrovirus which was the probable cause
of AIDS. The next day all papers wrote that a US researcher had discovered
the cause of AIDS. They had forgotten the word "probable"...
since then all research and therapy has taken place only from the view
of the virus hypothesis. In other words, for the past 17 years the question
has been researched: how HIV does cause AIDS; the question IF HIV does
cause AIDS must not be asked anymore.
Years later, Kary Mullis, Nobel laureate in chemistry 1993 and inventor
of the polymerase chain reaction, needed a reference for "the generally
known fact" that HIV was the cause of AIDS. While working on a project,
he became aware that he didnt know a scientific reference for the
statement he had just written down: HIV is the probable cause of AIDS.
So he asked the next virologist at the table after that basic paper. The
virologist told Mullis, he wouldnt need a reference in this case;
after all, everyone knows that HIV leads to AIDS. Kary Mullis disagreed
and thought such an important discovery should be published in some paper.
He learnt soon that it was impossible to find such a paper. Instead, he
was pointed to the press conference of 1983 over and over again.
One day, he got the opportunity to talk to Luc Montagnier from the Pasteur
Institute, the [claimed] discoverer of the virus, during an event in San
Diego. HE should know the answer. Confronted with Mullis´question,
Montagnier said: "Why dont you cite the report of the CDC (Centers
of Disease Control)?" Mullis answered: "This report doesnt
address the question whether or not HIV is the cause of AIDS" - "Right",
Montagnier admitted, "but maybe you could cite the SIV study (Simian
Immuno-deficiency Virus, which is very similar to HIV)." That paper
didnt convince Mullis either, because the monkeys developed different
diseases, also because the virus wasnt the same one, and thirdly,
because the paper had been published only a few months before. He looked
for the original paper that should demonstrate in whatever form that HIV
was the cause of AIDS. At that point, Montagnier's answer consisted of
running away, to greet a group on the other side of the room.
I had a similar experience this year  in South Africa on the AIDS
Advisory Panel, which had been initiated by President Thabo Mbeki. Mbeki
had invited 33 scientists from all over the world in order to shed light
on the AIDS problem in his country. Among these panellists were 22 scientists
who believed in the virus hypothesis. Furthermore, there were 11 so-called
dissidents (which I belong to), who cast doubt on the virus hypothesis
and rather assume that AIDS in Africa is the result of increasing poverty.
In the developed countries AIDS is the result of drugs, and above all
the result of the therapy against AIDS (AZT).
I asked Montagnier what convinced him that AIDS is caused by a virus.
Montagnier answered that over the years apparently an effective treatment
has been developed, and this was proof enough for HIV leading to AIDS.
In other words, the virologists have no virological arguments for the
theory that HIV leads to AIDS. Instead, they get the proof for their hypotheses
from physicians, who give a positive feedback by saying "Of course
AIDS is a viral disease that responds to antiviral treatment." However,
we doctors treat HIV-positive patients basically differently from if they
were HIV-negative. From shingles to apoplexy, HIV-pos. Patients are given
a lifelong antiviral treatment, or we treat them usually without any clinical
illness, only on the basis of surrogate markers like CD4-cells and viral
load, which (latter) can be measured via PCR (the method invented by Kary
Mullis). Mullis on his method: "It is nonsense to amplify something
that is detectable only by PCR and which is practically zero; it will
still be close to zero."
Now in Africa, on the panel, it also became obvious that the initial dose
of 1500-mg AZT (1987) was much too high. In other words, it became clear
that the situation of the patients then wasnt improved by this high
dosed therapy -but worsened. The high mortality of the AIDS patients at
that time was not too striking though, because it was the general expectation
that AIDS patients will die fast and young.
The problem of the therapy was and is that it is extremely immuno-suppressive
itself. AZT was developed in the 60s specifically as a chemotherapy against
cancer. But wasnt used then due to severe toxicity. However, a few
pre-studies had been carried out, so that the substance could be used
in the 80s. Then AZT was tested in a placebo-controlled study in 1987.
This study was cancelled after four months, because at that time it looked
like the patients in the treatment group would derive benefit from the
The publication in NEJM led to the world-wide use of 1500-mg AZT for AIDS
patients and HIV-positive people. The reason for the early cancelling
of the study was the unbelievable pressure from lobbying groups who hoped
a cure was found. But afterwards mortality in both groups jumped up and
reached levels of 80 - 90% after four years of AZT therapy. In other words,
after four years most AIDS patients had died.
This extreme mortality eventually got noticed though, and accordingly
the AZT doses were lowered around 1990, because it also became obvious
that the bone marrow couldnt stand the chemotherapy. Still, any
antiviral therapy has been and still is a lifelong therapy. Only this
year, after numerous problems with side effects were reported also for
the newer drugs (protease inhibitors), they publicly consider drug holidays
(Nature, Lancet, 2000). Now they state everywhere (see Montagnier) that
the new therapy works, because mortality of AIDS patients has clearly
declined. This, however, is nothing but a euphemism for lower toxicity
by dose reduction.
An increasingly critical attitude by patients themselves, who have witnessed
the AZT disaster of the early 90s and extensive literature on the AZT
problem have generated a more critical atmosphere toward the therapy.
And yet, declining mortality of AIDS is still attributed to the better
therapy, and declining mortality correlating with increased use of protease
inhibitors is demonstrated in a time frame (Palella et al. NEJM). What
you cant see in that time frame is the fact that mortality had already
been distinctly declining since 1990/91, the time when therapists noticed
that AZT in 1500 mg doses were not tolerable for their patients (bone
marrow suppression). At that time, however, we had already treated a whole
generation of AIDS patients into irreversible immune suppression.
This AZT catastrophe is the reason for the ineradicable belief that HIV
is the cause of AIDS. Moreover, it has led to the habit to use "HIV"
and "AIDS" as synonymous terms. Epidemiological predictions
are based on this assumption that HIV is the same as AIDS, and in respect
of all countries with such HIV-test explosions they predict that catastrophic
AIDS epidemics will follow. For the president of South Africa, Mbeki,
the discrepancy between what European and US newspapers write about his
country (drastic population reduction) and what is actually happening
in his country (doubling of the population within the past 30 years),
was striking. Hence he refused to follow the general (American) AIDS-politics
and instead, called the meeting of experts who had the task to examine
whether or not HIV was actually the cause of AIDS.
Two things had particularly startled him: First the extensive literature
on AZT and the damaging effects of this substance. Secondly a paper by
Max Essex that was published in the "Journal of Infectious Diseases"
and which describes a strong cross reaction of HIV tests with antigens,
that can be found in the bacteria which cause tuberculosis and lepra.
That means, nobody in Africa or elsewhere in the world knows whether a
patient suffers from tuberculosis because he is HIV-positive, or whether
he is HIV-positive because he suffers from tuberculosis.
Another problem of the AIDS epidemiology is the following: By now about
30 afflictions, all of which were known before, are being renamed to AIDS
in the presence of a positive HIV-test. This also is not an increase of
diseases of course --but just a redefinition. This circular definition
HIV+/TB = AIDS and HIV-/TB = TB makes the correlation HIV-AIDS appear
100%. For example, a patient who suffers from TB and who is also HIV-positive
is today considered an AIDS patient. A woman who suffers from cervical
carcinoma is today considered an AIDS patient, and so is a patient with
a lymphoma. If they have antibodies against HIV.
The virus-AIDS-hypothesis and the media alarm connected to it (12 cover
stories alone by the German magazine Der Spiegel) has caused the biggest
medical catastrophe and human tragedy, by driving countless numbers of
people into fear and despair, by causing suicides and iatrogenic deaths,
and is still doing so.
Possibly the end of this is in sight, if Mbeki will be successful with
his AIDS politics and will ban HIV-testing as well as antiviral medication
in his country, and instead, will fight tuberculosis that is progressing
in his country and poverty that is connected to it. Tuberculosis has always
been a good indicator for the weal and woe of a society (see the frequency
of TB in Germany after the two world wars, Statistisches Bundesamt Wiesbaden).
Modern tuberculosis however is now, after the introduction of HIV-tests,
called AIDS and is treated accordingly. In India they showed me patients
who had tuberculosis and sold house and home, in order to get the cure
(AZT) from the West.
With hepatitis C we see a similar phenomenon, although the iatrogenic
measure is not as drastic as in the case of the HIV/AIDS hypothesis. Here
one can only expect a temporary therapy with interferon and Ribavirin
, however this therapy too produces many side effects, and as I
will show, its also superfluous.
The birth year of hepatitis C is 1987. The laboratory for this job was
nothing less than the Chiron Corp., a biochemical company that by now
makes billions in sales with Hepatitis C tests. At that time they injected
blood from a patient with a Non-A/Non-B hepatitis into chimps. None of
the animals developed hepatitis. Just around day # 14 after the infection
they showed temporary increase of liver-enzymes (transaminase). The animals
were slaughtered, and the liver tissue was examined. They didnt
find a virus. Being in deep despair they then searched for the tiniest
traces of a virus, and amplified a little piece of genetic information,
that didnt seem to belong to the genetic code of the tissue, via
PCR. They assumed that this piece of foreign RNA must be the genetic information
of a before undiscovered virus. Whatever it was, the liver tissue contained
it in hardly detectable quantities, but they were able to build an antibody
This antibody bestowed us the hepatitis epidemic insofar, as test explosions
are taking place again and HCV positive patients are now told they carry
a virus that after a latency period of ca. 30 years will generate a liver
cirrhosis. Most of the HCV positive patients, however, dont have
any symptoms of illness. Some have slightly increased transaminase, and
real liver damage is almost exclusively a problem of those patients who
have consumed alcohol and drugs before. Here we see indeed a big overlap
insofar, as almost 80% of the drug addicts are HCV positive. Now we have
to answer the question again, does the virus damage the liver, or the
drugs and the alcohol? The 30-year latency period would then be an euphemism
for the toxic effects of drugs and alcohol that can lead to liver cirrhosis
after 30 years.
While two or three years ago newspapers had headlines like "Hepatitis
C - underestimated danger; HCV - unrecognised danger; HCV - the new big
plague, "It comes quietly but powerfully". We nowadays read
more often: "Danger of hepatitis overestimated?". Prof. Manns
from Hannover, who initially was one of worse case predictors, is now
saying that - based on the available studies and on a cost-benefit-risk
estimation - therapy for Hepatitis C can be seen as a relative counter
This new view when it comes to an estimation of hepatitis C has the following
background: Last year Seef et. al published a big study in Annals. of
Internal Medicine, that was carried out with GIs whose serums had been
frozen 45 years ago. A follow-up over 45 years showed that there are practically
no differences between liver diseases of HCV positive and of HCV negative
This indeed leads to the consideration that the risk of a HCV positive
person developing liver cirrhosis later in life was apparently massively
overestimated. And it makes the theory appear more plausible that liver
toxic substances like alcohol and drugs, called "cofactors",
are actually the main factors. Hence, a positive HCV test obviously has
no clinical relevance. Accordingly, antiviral treatment for HCV positive
patients doesnt make any sense.
Moreover, medical treatment of liver diseases has been considered paradoxical
by leading hepatologists over many decades, because practically all substances
damage the liver in one way or the other, because the liver is the main
organ for metabolism of toxins. For example, Benuron, that is used during
an interferon treatment one gram per day. Remember in this context the
Fialuridine disaster - a treatment attempt - a few years ago, where a
couple of patients died, and others could only be rescued by liver transplantation
(Hoofnagle et. al).
A German scientist and his team were able to find the sequences named
HCV in human DNA of healthy HCV negative individuals. So, its imaginable
that HCV positivity can be produced endogenously when liver cells get
damaged by toxic substances like alcohol or drugs and then generate these
sequences. This would explain the relatively strong correlation between
HCV positivity and alcohol/drugs.
In the case of hepatitis C its similar for hepatitis G - we can
apparently still hope for a self-correction of science, because of the
lack of clinical evidence. HCV positive liver cirrhoses occur almost exclusively
in drug users or alcoholics, while a significant group of people who are
HCV positive and develop a liver cirrhosis at the age of 50 and who are
free of nutritive-toxic liver damages, does practically not exist.
Medical publications and the general press are promoting the epidemic-like
character of the hepatitis C plague. Recently, in Itzehoe a HCV positive
surgeon allegedly infected many of his patients. But one has to consider
that prevalence of hepatitis C antibodies is relatively high in the population,
so that it is easily possible that 2% react positively to HCV tests, that
means 40 cases out of 2000 would match the general degree of "infection".
BSE (Bovine Spongiform Encephalopathy)
Now the atmosphere of plague fear culminates in the BSE hysteria --where
we have not one case of illness in our country [Germany], and still you
can read about the BSE crisis or BSE plague in all newspapers. Here again
we see the phenomenon of a test explosion, insofar as the Swiss company
Prionics has their BSE tests ready for the market and is distributing
them. Here again a positive test case is equated with a case of disease.
The plague atmosphere created by this is even supported by the panic which
comes up with the hypothetical notion that mad cow disease can be transmitted
to humans by them eating beef and will appear as the new variant of the
Creutzfeld-Jakob disease. The media heat up this atmosphere of plague
fear by dragging putative victims in front of the TV cameras although
the disease is only diagnosable post mortem.
While all epidemiological data available so far contradict such a connection,
this is still the big fear, which drives scientists and politician to
the current totally overdone safety measures (mass slaughter of cows).
If we want to understand this fear, we must browse back a some years,
and consider the work of Carleton Gajdusek. Gajdusek did research in Papua
New Guinea in the 70s, on a kind of dementia, which was prevalent mainly
in the female population there. The disease Kuru was observed as being
endemic in two tribes whose members often married each other. These so
called transmissible spongiform encephalopathies which Kuru belongs to,
the Creutzfeld-Jakob disease, the familiar insomnia and the Gerstmann-Sträußler-Scheinker
syndrome appear sporadically or genetically caused and of autosomal dominant
origin. These diseases are fatal within 5 years. They are extremely rare,
frequency is around 1 : 1000000 and within a family with a frequency of
1 : 50 --which is a good argument for a genetic cause.
But Gajdusek received the Nobel Prize for his concept of slow viruses
and thereby established the transmissibility of those spongiform encephalopathies.
However, if we observe his experiments he tried to prove the transmissibility
with, we have to wonder today that the scientific community at that time
accepted those papers as proof for transmissibility.
Neither the feeding of infected brain tissue nor the injection of it affected
the lab chimps, only one bizarre experiment led to neurological symptoms
in the chimps, and this was intra-cerebral inoculation experiment. On
these experiments the transmissibility of those diseases is based! Hardly
evidence for Gajdusek´s cannibalistic hypothesis, which postulates
that the disease in humans could be caused by the consumption of, infected
brain. Burdensomely we have to add that Gajdusek is the only witness alive
for cannibalism in Papua New Guinea. One teams of anthropologists that
examined the case, found stories about cannibalism but no authentic cases.
So, about Gajdusek´s Nobel Prize we can only say, if his stories
are not true, they have nicely been made up anyway. Despite these inconsistencies
(intra-cerebral inoculation experiments) for proof of the oral transmission
path the notion of oral transmission is now so established that we actually
fear the consumption of beef. According to Gajdusek´s attempts,
we would only have reason to fear something, if we made holes in our head
and inoculated the infected brain of mad cows.
Also on the cannibalistic hypothesis the assumption is based that by feeding
of infectious animal meal the plague got started. Because of the general
acceptance of this hypothesis it is entirely neglected that the epidemiology
of BSE does not match the feeding of animal meal at all. Great Britain
for instance has exported tons of animal meal to the Middle East, South
Africa and also to the USA. In none of these countries BSE occurred Instead,
BSE cases almost always occur in Great Britain (99%), Switzerland and
One explanation is in the case of BSE again the intoxication hypothesis.
1985 in England a law came into force which forced British farmers to
pour Phosmet along the napes of their cows. Phosmet is an organphosphate
that is used as insecticide against the warble fly. This substance was
used in relatively high concentration only in Great Britain, North Ireland
and Switzerland, and the law didnt allow an exception. A British
farmer, Mark Purdey, noticed that his cows from organic production didnt
develop BSE although they were fed by animal meal, but never treated with
The British Government knows this context, and in the early 90s the law
was taken back, because a connection between the organophosphate and the
occurrence of BSE was very likely. Organophosphates can change the alpha
helix structure of proteins. According to this measure, BSE cases started
to decline from 1993 on. Actually, the British inquiry committee admits
that organophosphates are apparently a cofactor for BSE. Toxicologically
it is known (Lüllmann, Kuschinski: Lehrbuch der Toxikologie) that
chronic intoxications with organophosphates lead to "the clinical
symptoms of polyneuropathy. The basis is axon swellings and fragmentation
and eventually demyelinization of peripheral and central axons".
However, the BSE inquiry committee refuses to accept the organophosphates
as the sole cause. But one question comes up. Why do not all those cows
get the disease that was treated with organophosphates? Here we must consider:
The dose makes the toxin - and even if all cows get the some quantity
it depends on the diffusion distance whether the toxin reaches the central
nervous system and can start its damaging activity.
Thereto the observation of British farmers: meagre milk cows are significantly
more receptive to BSE than the fatter beef-cows. If one pictures the diffusion
distance the nerve toxin takes after being poured over the nape of the
cows, one can easily imagine that the thickness of the subcutaneous fatty
layer is quite crucial for whether or not a cow will develop BSE. As lipophilic
substances the organophosphates are buffered in the subcutaneous fatty
But if a toxin can speed up the outbreak of a disease, like alcohol can
contribute to liver diseases, then it can also be the sole cause. However,
if Phosmet would be declared as cause of BSE, compensation lawsuits in
billions would wait for both the British government and the manufacturer
of the insecticide. This is certainly not desirable for them, so they
prefer to surround the basically clear context in a fog of prions.
Intoxication hypotheses are easily testable and in contrast to the virus
or prion hypotheses also falsifiable. They can be examined toxicologically
and epidemiologically and then we can either accept or reject them.
For AIDS, the intoxication hypothesis would make following predictions:
All patients, who die young of AIDS, must have used recreational or antiviral
drugs over a longer period. There must not be a significant number of
people who die of AIDS at a young age and who are drug free and havent
taken any antivirals.
For hepatitis C it would mean, that there is no significant number of
people who die of Hepatitis C caused liver cirrhosis in their midlives
and who are drug free and alcohol free.
And for BSE the intoxication hypothesis would mean that only cows who
have been treated with organophosphates, develop BSE, and inversely, if
a significant number of cows with no organophosphate treatment would develop
BSE, the intoxication hypothesis would be proven wrong.
As elaborated above, epidemiological and toxicological data suggest that
chronic intoxications are the real cause for the named diseases AIDS,
HCV and BSE. Why these plausible hypothesis arent investigated further,
this is a topic one could write a book about which could have the title
"conflicts of interests".
Infection hypotheses can help making billions of dollars:
1. The antibody business: Millions of screening tests are distributed,
each blood sample needs to be tested (4 millions in Germany alone)
2. The therapy business: Antiviral medication, 3 or 4 or 5 fold combinations,
AIDS cant be topped in this department.
3. Possibly vaccinations: Here, however, the concept of the new big plagues
gets in the way of itself, because this has brought up the central paradox
of immunology. Since the beginning of HIV they have told us: He who has
antibodies to HIV, will die, instead of, he who has antibodies to HIV
will live, which would meet our vaccination concepts. How many HIV antibody
negative individuals would like to get vaccinated, in order to have antibodies
to HIV afterwards?
With intoxication hypotheses on the other hand you cannot make any money
at all. The simple message is to avoid the poison and you wont get
sick. Such hypotheses are counterproductive insofar as the toxins (drugs,
alcohol, pills, and phosmet) bring high revenues. The conflict of interests
is not resolvable: What virologist who does directly profit millions from
their patent rights of the HIV or HCV tests (Montagnier, Simon Wain-Hobsen,
Robin Weiss, Robert Gallo) can risk to take even one look in the other
What physician who has treated AIDS or hepatitis C patients over many
years in good faith in the virus hypothesis and with high personal input,
can look in the other direction? The more so as he must get the feeling,
due to seemingly plausible changes of surrogate markers, that he is on
the right track. Everywhere in the world children are treated according
to this principle. Healthy children get antiviral therapies, in order
to "delay the outbreak of illness", that is, a clinically healthy
HIV pos. child gets a therapy, and any affection that appears under this
therapy will be blamed on the "basic disease" or interpreted
as therapy failure because of the virus developing resistance. In other
words, the child has no chance to escape.
I have experienced myself --at a trial in Canada (I was ordered to as
an expert of AZT), how healthy kids were taken away from their mother
who had been HIV+ for 15 years and who was allowed to refuse anti-retroviral
treatment for herself but not for her children.
Similar was a judicial sentence in England where a HIV positive couple
refused to get their newborn tested. The judge said that the child must
be tested, because in the case of a positive test result immediate therapy
would be necessary.
Even study results that shed light on the AZT use of pregnant women arent
able to wake up the authors. They describe a 5 - 6-fold higher risk of
a rapidly progredient course of HIV infection for those kids whose mothers
have been treated with AZT during pregnancy, compared to children whose
mothers have not got any AZT (J. of AIDS, 2000). At least our efforts
in Africa on the panel seem to have somewhat impressed the Americans,
because a few weeks ago the NIAID (National Institute for Allergic and
Infectious Diseases) announced a big multi-centre study that included
a therapy branch without antiviral therapy. So, after 13 years of aggressive
long term therapy now a "U-turn" over to what until now has
been considered not justifiable - a real placebo control with clinical
endpoints, planned for four years.
It would be my wish that I have seeded at least a few doubts with my lecture,
and I hope to inspire a broader discussion.
The original article has been written for a lecture for doctors in
Kiel, Germany. It has been published in English at: ?????
The author can be contacted at: <Koehnlein-Kiel@t-online.de>