The blockade of the respiratory enzyme cytochrome oxidase by AZT prevents
conversion of electrons into O2. The immediate result is reduced ATP production and
an increased synthesis of toxic oxygen radicals. The cells suffer from loss of energy.
Within a few minutes and at latest within three hours, there is a reaction to the AZT
that cannot incorporate in the DNA. Meanwhile, replication of the DNA nucleus or any
kind of DNA provirus (that always depends on DNA nucleus replication of active cells)
would require 40-72 hours according to the theoretical build-up of AZT-TP. The
blockade of oxygen respiration and energy production in T-helper lymph cells (T4 cells
or CD-4 cells) resulting from AZT medication leads specifically to premature death of
immune cells or, under certain conditions in accordance with the law of nature to
switching of maturing T-helper immune cells to type 2 T-helper immune cells (TH1-TH2
switch) as part of a type II counter regulation.
Both reaction forms result in immune system weaknesses. The premature dying
particularly affects TH1 cells. Their depletion is the principal immunological
characteristic of so-called HIV-positive and AIDS patients. It is the function of TH1
cells to eliminate intracellular pathogens such as parasites, fungi, mycobacteria, and
viruses. Since the discovery of nitric oxide (NO) production in human cells (Furchgott
and Ignarro, 1987, Nobel Prize, 1998), it has been beyond any reasonable doubt that
NO gas production in TH1 cells is indispensable for elimination of intracellular
pathogens. If the TH1 cells producing NO gas are lacking, opportunistic pathogens may
develop (AIDS). The function of the TH2 cells is to prompt antibody formation. TH2
cells produce no NO gas to eliminate intracellular pathogens.
Numerous studies have proved that so-called HIV-positives show a loss of TH1 cells
and a dominance of TH2 cells at the earliest possible stage in so-called HIV
seroconversion. It is biologically unimaginable that all T-cells should be settled at the
stage of the so-called HIV infection by HIV, since the prevailing TH2 cells are intact,
and antibody production is even increased. The TH1-Th2 switch, which leads to
cellular immunity weakness, must therefore have other causes according to the laws of
logic.
The active mechanism of NO and AZT (=N3) is identical: inhibition of cytochrome
oxidase in complex IV of the mitochondria respiratory chain is the essential physically
and patho-physiologically active factor in human cells through NO and also AZT.
Depending on duration and dose of increased NO production as well as medication of
AZT, special cell types and disposition of patients, a concurrent rise occurs in cell
death (apoptosis, necrosis) and/or TH2 cell dominance (opportunistic infections =
AIDS), tumor formation (e.g., Kaposi’s sarcoma, lymphoma, carcinoma), or
degeneration of the skeleton and heart muscle cells as well as nerve cells).
The causes of AIDS in Western countries have been clarified epidemiologically and
patho-physiologically without any reasonable doubt in thousands of experimental and
clinical studies. Without any doubt, unusual accumulating load factors for exogenously
and/or endogenously induced NO over-stimulation have been proved in all so-called risk
groups. There is no rational, comprehensible biological reason to assume that the
combination of these immune stress factors in Western civilization should have
remained completely ineffective and without recognizable disease results. Strong or
lasting NO over-stimulation leads as a counter-reaction to increased cell death and/or
in the case of T-helper cells to TH1-TH2 switch with inhibition of the cellular
production of NO and disturbance of the mitochondria’s oxygen respiration.
The clinical results (including AIDS) are in no way puzzling but rather programmed in
accordance with law of the biology of evolution. The so-called HIV ( the virus that
nobody has actually isolated so far according to the standard rules of retrovirology and
that was deduced to exist only due to unspecified molecular markers to postulate it
hypothetically as cause of disease( is neither sufficient nor necessary. This postulate
veils the real cause of AIDS. At the point in time when the "HIV causes AIDS" disease
theory was developed, the researchers did not know of NO production in human cells
or the existence of two forms of T-helper immune cells with and without NO gas
production. Nor were we aware of the dependence of the function of eliminating
intracellular pathogens to TH1 cells and their NO gas production or of the regulation of
oxygen respiration in the mitochondria by NO and its derivatives. Failure to consider
these research data by HIV/AIDS-researchers can only be based on ignorance or
unwillingness to learn.
This explanation of AIDS’ causes and the active mechanism of AZT is supported by the
fact that after introducing clinical medication in malignant forms of lymph cell cancer
with substances analogous to nucleosides (that show the same active mechanism as
AZT), a massive loss of TH1 cells appeared in the same form among all treated, and so
did the inverse ratio of T4/T8 lymph cells and opportunistic infections. Exactly these
immunology data and clinical symptoms define the AIDS syndrome. Since presentation
of the conclusive data from NO research, cytokine research, mitochondria research,
and other experimental and clinical research sectors from the mid-1990s, there are no
longer grounds for rational doubt about the actual causes of AIDS in Western
countries.
African clinical standards for diagnosing AIDS and test-procedure standards for
antibodies against the so-called HIV are in no way congruous with those of Western
countries. However, regardless of race and country-specific diagnostic practices, all
human beings are identical in the response that evolution has programmed into human
immune and non-immune cells when affected by nitrosative and prooxidative stress
conditions.
In Africa it is particularly chronic inflammatory and infectious processes, protein
shortages, and malnutrition (nutritional AIDS), contamination of drinking water with
nitrifying bacteria, and nitrosamine burdens in nutrients that can lead to clinical
symptoms of opportunistic infections (AIDS) as result of induced TH1-TH2 switches.
Chronic infections stem from (1) mycobacteria, such as chronic tuberculosis or the
leprous form of leprosy, (2) spirochete bacteria such as the tertiary form of syphilis,
(3) malaria pathogens, trypanosomal, toxoplasmic, and other parasites, (4) fungi
pathogens such as pneumocystes, candida forms, histoplasms, crytococcus, and many
others. These always result from too weak a TH1 immune response and a switch in the
TH1-TH2 immune cell balance to TH2 immune state with increased antibody
production. Infections such as worm parasites trigger a priori a TH2 immune response
that can become chronic.
If the clinical symptoms of unspecified sort and duration become chronic, these have
been diagnosed in Africa since 1985 as AIDS, based on the Bangui definition, without
test evidence of so-called anti-HIV antibodies. This pragmatic procedure led to the
apparent proof of a suddenly rapid increase in Africa of so-called HIV-caused AIDS
indicator diseases.
Arbitrary projections from small random samples of so-called HIV-positive serum tests
and sweeping clinical AIDS diagnoses in Africa still serve the World Health Organization,
UNAIDS, the Western countries, and the international news media as basic proof of the
HIV pandemic in Africa and the threat deduced from that pseudo medicine it poses to
all humanity.
Since children, women, and men can suffer from chronic inflammatory and infectious
processes due to general living conditions in developing countries, these AIDS cases
can be manipulated at will in terms of sweeping medical statistics as proof of
heterosexual transfer and mother-child transfer leading to the so-called HIV in Africa.
Since these undoubted facts are logical in view of the high scientific standards of
Western medicine and can be understood with little intellectual effort, there is no
rational reason to assume that it involves a tragic scientific error in case of an
intended mass poisoning with the proven mitochondria inactivator azidothymidine
(AZT). No HIV-AIDS researcher and no medical specialist to date has been able to
answer the inescapable medical-ethics question of why medicinal application of AZT
and other substances that trigger the loss of TH1 immune cells, reverse the ratio of
T4/T8 lymph cells, and opportunistic infections should be indicated to treat patients in
danger to develop Pre-AIDS and AIDS.
That AZT is effective as inactivator of mitochondria can be derived from the bio-logical
fact that azidothymidine was isolated from herring spermatozoa in 1961. The
spermatozoa of vertebrates are not allowed to transmit these cellular symbionts to the
feminine ovum, and to be activated before penetration to the feminime ovum and the
mitochondria of the spermatozoa must be inactivated at the time-point of penetration
into the ovum. In the case of vertebrates, only the mother's cellular symbionts will be
transmitted to daughter cells. AZT was produced synthetically in 1964 but banned
from human trials after tests on mice and rats diseased with leukemia resulted in
developing lymph-cell cancer. AZT was used clinically for AIDS patients from 1986 on,
but without evidence of its actual incorporation in any provirus DNA and without
testing for possible mitochondria damage.
The question if AZT can stop replication of the so-called virus is inseparably linked with
the question concerning evidence of the so-called virus.
The so-called anti-HIV antibody test has been stocked with nitrosatively and
oxidatively stimulated human stress proteins as antigens from lymph cell cultures of
patients manifesting AIDS and from co-cultivated lymphatic leukemia cells. The test
substrates have been calibrated so that a positive test result will particularly appear
from a certain amount of unspecified antibodies which in the blood serum of test
subjects characteristically indicate an outlasting TH2 immune-cell response and an
increasing antibody reaction. The test reaction level and the number of test antigens
in the so-called anti-HIV antibody tests have been determined arbitrarily. For this test
reaction level and the required test-antigens there are no internationally obligatory
standards. In Africa, for example, a reaction in so-called HIV tests is usually rated a
positive test result with fewer and different test antigens than in Western countries.
Since no antibodies form in the human immune system that react only with those
antigens against which they were originally formed, the statement that so-called
anti-HIV antibody tests react exclusively with antibodies formed in human organisms
against antigens of the so-called HIV is already objectively in error for this biological
reason. So-called HIV test antigens, for example, react demonstrably with antibodies
against tuberculosis, malaria, and pneumocystis pathogens as well as many other
antibodies against microbial and non-microbial antigens.
In Western countries too, applied determination of so-called viral load with the help of
the PCR laboratory technique is completely unsuitable to detect the so-called HIV’s
RNA according to the inventor of this DNA-multiplying method, the Nobel Price laureate
Kary B. Mullis. Nobody to date has actually isolated a natural RNA sequence or a
provirus DNA sequence of so-called HIV. All publications on the so-called isolation of
so-called HIV show nothing else than findings of unspecified molecular markers that are
arbitrarily interpreted as "finger prints" of the so-called HIV.
Other data of scientific findings can not be expected in view of the pressing
epidemiological, immunological, cell-biological, and clinical proof situation that type II
counter-regulation of human immune and non-immune cells as well as development of
AIDS-indicating diseases are evolutionary programmed under certain conditions. For
physiological and patho-physiological understanding of these immunological and clinical
phenomena, the assumption of an infection with so-called HIV is neither sufficient nor
necessary but objectively redundant. It was assumed at the conference of leading
HIV-AIDS researchers in 1997 that no disease mechanism of the so-called HIV could be
proved (M. Balter, 1997; Science 278: 11399-11400).
The question is often raised whether AIDS could be transmitted in another way,
sexually, into the bloodstream, via the respiration system or other infection routes if
one assumes that the so-called virus is not the cause of AIDS.
Many people have mental difficulty in separating certain facts of the immune system,
since it is suggested to them that the immune cells of so-called HIV-positives and
AIDS patients react primarily to infectious pathogens that are usually transmitted
sexually from a so-called HIV-positive mother to her children. However, the biological
truth is that human immune cells are influenced by a number of non-microbial immune
stressors as well as microbial immune stressors (antigens and toxins). Thus AIDS
indicator diseases must not always be triggered primarily by infections of any kind, as
demonstrated by the examples of nutritional AIDS, transplantation AIDS as a result of
immunosuppressive therapy, or by AIDS after AZT medication or after medication with
other nucleoside analog drugs.
A homosexual African, for example, can also become ill of nutritional AIDS, even if he
never takes the risks of an anal-receptive homosexual from the West. However, he
would be registered in Africa as a heterosexual HIV-AIDS patient. Nor would the
apparent mother-child transmission of AIDS have to be caused primarily by infection in
any way. Since the immune cells and non-immune cells of the fetus show a dominance
of TH2 or type 2 cytokines respectively during pregnancy, the disposition for
opportunistic infections after birth (AIDS) depends mainly on whether the mother has
transmitted enough intact maternal antibodies and a stable TH1-TH2 immune cell
balance can be adjusted in the child during the first months of life.
In case of the mother lacking nutrition, being poorly nourished, or suffering toxic
damage before and during pregnancy, the maturing of the infant’s T-helper immune
cells will be substantially affected. Opportunistic infections (PCP) were already
diagnosed during the 1940s among prematurely born children and orphans in Europe.
Opportunistic infections also appear among children with congenital thymic aplasia.
That children of nutritionally, infectiously, and toxically damaged mothers in Africa
should suddenly be infected by so-called HIV if they develop opportunistic infections
cannot be comprehended rationally, not even if the so-called anti-HIV antibody test
shows a positive result for the reasons mentioned above. Treating such children
preventively or therapeutically with AZT or other nucleoside analogues would then be
inhumane treatment in the sense of the UN Declaration of Human Rights ( even when
one works from the assumption that the postulated so-called HIV would exist and
would be transmitted from mother to child. The restricted or unrestricted treatment of
the not yet matured immune cells of a newborn child by means of substances that
demonstrably largely damage the maturity of immune cells fulfills the facts of the case
for deliberately inflicting bodily harm with fatal results and must be condemned as
especially inhumane treatment internationally.
President Mbeki’s questions to the conference of experts on 6-7 May 2000 in Pretoria
show the basic misunderstanding that arises from viewing AIDS as the exclusive result
of a sexual infection and taking no account a priori of all other immune stressors
(whether or not sexually associated, infectious, or noninfectious). For example, more
than 90% of those older than age six in Western countries indicate/show antibodies
that also react to pneumocystes. But only a few human beings fall ill of pneumocystis
carinii pneumonia (PCP), the most frequent AIDS-indicating disease in Western
countries. The pathogen is a fungus that is transmitted airborne from person to
person. If a human being becomes diseased from such an opportunistic PCP, it depends
entirely on whether enough TH1 immune cells are available to produce the cytotoxic
NO gas in order to eliminate PCP pathogens after specific signals from antigen
presenting cells and toxin stimulation through pathogens. In case of the disease, the
PCP pathogens benefit from cellular immunity weaknesses, regardless if the precedent
TH2 dominance was resulting from stressors, that were infectious or noninfectious,
sexually transmitted or not.
Gender and manner of sexual transmission may play a role, but they may just as easily
not be a factor. Other pathogens that trigger opportunistic infections may gain
advantage from previous chronic infections, even though they produce no
opportunistic infections themselves. One knows such interactions in Western countries,
for example, among surgical patients after operations and trauma as well as among
patients in intensive-care wards. Such interactions of chronic and opportunistic
pathogens are frequent in developing countries. They may have nothing to do with
so-called HIV, not even if the so-called HIV-test is positive and the T4 cell count is
low. On the contrary, such laboratory findings can be given in case of any marked TH2
immune-cell dominance and existing chronic infections without the presence of any
so-called HIV. However, an AZT medication would even be counter-indicated if the
existence of the so-called HIV were proved, since such so-called HIV would only die
with the immune cells and because it would kill more immune cells that were not
infected with the so-called HIV. But these biological conditions do not mean that AIDS
is "transmitted", since AIDS is the clinically resulting syndrome and not the cause of
the acquired TH1 immune cell weakness and the inhibition of toxic resistance-gas
production. Transmitted are pathogens that can primarily be involved in developing a
TH1 immune weakness or can profit secondarily in case of an existing TH1 weakness.
Yet even among homosexuals, these transmissions in no way result only via the sexual
channel but though all possible access channels.
The superficial differentiation between heterosexually and homosexually associated
transmission of so-called HIV serves Western HIV/AIDS propaganda as a manipulative
suggestion of a fatal so-called HIV infection transmittable to anybody through sexual
contact. It ignores infectious immune stressors and involvement of non-infectious
immune stressors, trivialised as cofactors (which have been very effective disease
triggers for millions of years without so-called HIV). However, the predominantly
homosexual transmission of so-called HIV infections in Western countries and the
heterosexual transmission of so-called HIV infections in African countries are not
explained by HIV/AIDS researchers as result of special infectious and non-infectious
risks of a minority of homosexual patients and the general living conditions in Africa
countries but as a result of the demonstrably special sexual compulsiveness of
homosexuals and African men and women.
During the past 15 years the international mass media have omitted no abnormal cliché
on the fantasized sex lives of African men and women. In order to avert the alleged
pandemic for all humanity, it is demanded quasi in sheer solicitousness that pregnant
women and newborns in Africa be treated with AZT. As start-up help and for seemingly
humanitarian reasons, pharmaceutical concerns in cooperation with the WHO and
Western countries are offering AZT and other nucleoside analogues at dumping prices.
The crucial question in this economic who-done-it is no longer if AZT can stop
so-called HIV but if South Africa can serve as the gateway for AZT in developing
countries.
A problem that first came to public light through the change in knowledge of medical
research during the past decades is intensifying for Western countries as well as
developing countries: the increasing abuse of chemo- antibiotics and mass vaccination
since the end of World War II. Both factors can favour a predisposition for the
long-term prevalence of TH2 illnesses such as allergies, ectopic skin diseases, chronic
arthritis, certain autoimmune diseases, AIDS, cancer, etc. The reason for this is the
lack of training on TH1 immune cells and the shift in the balance of TH1-TH2 immune
response. An indicator for this two-edged change in the infectious load profile in
Western countries is the fact that practically only patients from age groups born after
World War II were diagnosed as AIDS patients. The same applies to patients with
organ transplants (without genetic disposition) who have developed transplantation
AIDS. This acquired disposition has an even graver impact under the general living
conditions in developing countries than in Western countries where the change in
disease has already been clearly recognized in the growing number of chronic diseases
compared acute illnesses.
During the ongoing decade, evolutionary biology laws of co-evolution must be
discussed anew in light of medical research’s fundamental findings in the 1990s. A
future-oriented and rationally based health-care and social policy must be oriented
within this context ( not in the context of irrational theories that have caused the
waste of enormous scholarly and economic resources.
Heinrich Kremer, M.D., medical director emeritus, head of social therapy for addicts,
sexual offenders, and people with personality disturbances at Berlin Tegel (pilot project
of the Federal German government on reform of the penal system) retired from federal
service in 1988 as medical director of the clinic specializing in youth and young-adult
drug addiction (model study of the federal government in Brauel, Lower Saxony) due to
differences on medical and professional ethics in regard to drug and AIDS policy. Since
1988 he has worked in basic research on cancer and AIDS, from 1995-1999 with Prof.
Alfred Hässig as a cooperative member of the Study Group Nutrition and Immunity
(Berne).