TERAPIA NON TOSSICA per l’AIDS
Non-toxic AIDS therapy (English)
New letter with articles on the test and on the epidemy
Study Group AIDS therapy – c/o Felix de Fries – Eglistr. 7 CH-8004 Zürich
To those affected, To groups and institutions and to media all over the world – Zürich, 19th July 2002
Non-toxic AIDS-therapies: The Congress of indipendant scientist, medical doctors, groups and activists paralell to the World AIDS-Congress in Barcelone.
Dear Sir or Madam
Various studies on AIDS related topics, carried out since 1990, demonstrate:
– that cell cultures of cells from AIDS-patients have been co-cultivated with leucemic and embrional cells and have been activated with cortison to induce a higher rate of reverse transcription when the new HIV-retrovirus was postulated in 1984 and the HIV-antibody tests were formulated.
– that the postulated HIV-retroviruses untill today have not been isolated, photographed or characterised biochemically according to the established rules in virology and therefore have not been demonstrated to be transmitable, infectuous pathogens. After two illnesses (PCP and Kaposi Sarcoma) that originally defined the AIDS syndrome many more illnesses (e.g. tuberculosis, herpes, candidasis, toxoplasmosis, lymphoma) were declared to define the AIDS syndrome ( often even without the administration of HIV antibody-tests, that were defined in a different way in African countries than in Europe and USA). This was done to postulate a world-wide HIV epidemy.
– that antibodies bind to various antigens and that it is impossible to define to what sort of antigen an antibody primarly was formed. Therefore a positive result in the HIV-antibody tests only demon-strates a enhightened amount of polyspecific antibodies which passes a certain level. This antibodies are transmitted from the mother to her child.
– that it was known already in1984 from trials with leucaemia patients, that nucleosid analoge drugs namely AZT effect a lasting decrease of CD-4 and CD-8 cells and the inhibition of cellular immune reactions (the destruction of cells containing viruses, fungi and mycobacteria by killer cells), and that they induce thereby the emergence of opportunistic infections (e.g. PCP, toxoplasmosis, cytomegalo viruses, herpes), that can define the AIDS syndrome.
– that it was demonstrated in 1990 in various animal trials, that nucleosid analog drugs such as AZT cause severe damage to the mitochondrial DNA not only in bacteries and viruses but also in the mitochondria of the human cells, thereby causing irreversable damage to the bone marrow, the brain, the muscles and internal organs. This damage in the mitochondrial DNA is herited from the mother to her child.
– that it was known in 1980, that the unlimited use of chemoantibiotics (e.g. TMPSMX, Septrime, Co-trimoxazole) used often in the therapy of veneral infections cause damage to CD-4 and CD-8 cells and to the mitochondrial DNA respectively an overexertation of the antioxidantive redox-system in cells. (Many of this antibitoics, forbidden in western countries, are administrated in the countries of the developing world.) It was also known, that this antibiotics by an uncontrolled administration cause multiresistant strains of bacteries and the occurence of opportunistic infections. (This infections occuring first in urban gay men in the USA, who frequently used this antibiotics and NO drugs (nitrites) then were traced back to the postulated HIV
– that a lack of glutathione molecules in antigen-presenting cells and a lack in NO-gas induce the formation of CD-4 to cells with the Th2 zytokine prophile. This cells move to the bone marrow, where they stimulate the production of antibodies against external pathogens, whereas the cellular immune reactions (dedection and destruction of cells containing viruses, fungy and micobacteria), activated by CD-4 cells with the Th1 cytokine prophile, are continuously inhibited.
Studies since 1989 have demonstrated that positive HIV-antibody test results and AIDS-defining illnesses only occur in persons that show a lasting lack of gluathione molecules. Later it was demonstrated that this lack in glutathione moleclues can be replenished by the administration on N-acethyl-Cysteine, used in the for the syntetisation of glutathione molecules.
– that malnutrition is the principal cause of immune deficiency. The lack of proteins (containing methionine), amino acids, fatty acids, vitamines and trace elements leads to weake immune reactions and to deficient formation of the thymus gland in the childhood. Malnutrition with to few proteines, a lack in antioxydants (fresh fruit and vegetables), to much refined carbon hydrates (sugar, white flour) and humid cereals (that contain fungy, producing toxines) weakens the immune system.
– that dirty drinking water causes frequent bacterial infections that continuously activate the production of antibodies against external pathogens, whereas the dedection and destruction of cells containing viruses and myccobateries is continuously inhibited.
– that with the supply of N-azethyl cysteine, herbal antioxydants, heparines, essential fatty acids, amino acids, vitamines, trace elements and co-enzymes an effective, non toxic treatment of AIDS defining illnesses can be achieved.
Since 1985, when the HIV-retroviruses were postulated to be the cause of the various diseases that can define the AIDS-syndrome, the representatives of an international AIDS-establishment have anounced year by year that an effective antiviral treatment and an effective
HIV-vaccine would be soon available and that only a few more tests and experiments must be carried out to find it. The lethal effects of this antiretroviral treatment were traced back to the postulated HIV retroviruses.
Year by year it was announced that the adverse effects of this substances could be diminished by new formulas.
All this attempts to treat AIDS defining illnesses with nucleosid analog drugs to suppress the replication of the fix pathogenic parts in the DNA of the cell nucleus, considered according to the model of gene therapy to be the cause of this diseases, have failed. Thousands of persons with a positive result in HIV-antibody test have found death since 1985 by the lethal effects of the nucleoside analog drugs and synthetic protease inhibitors administrated. (The diminished doses of nucleosid analog drugs first lead to a fast decrease of the mortality in AIDS patients, but soon the s.c. resistance and the severe toxic effects of the Haart
therapy (liver failure, heart attacks, mitochondrial disfunctions) were occuring.
The producers of this toxic substances and of the various HIV-antibody tests made billions of dollars of profit, while most of the antiviral AIDS research was financed by public institutions. Today the CDC and the Massachusetts Institute of Technology warn of gene mutations and other severe toxic effects of HAART therapy composed by nucleoside analog drugs and synthetic protease inhibitors.
At the moment they carry out large human trials with so called HIV-vaccines, coordinated by the CDC in Atlanta. With the administration of a so-called HIV-vaccine, made of nacked DNA, they try to induce the formation of a high rate of polyspecific antibodies, that should lead to a positive HIV-test result in previously negative tested persons from risk-groups. With this effect they try to demonstrate that with the formation of this “HIV-antibodies” a better defense against an external infection with this postulated retrovirus can be achieved. (Earlier they considered the so-called HIV-antibodies as markers for an inevitable
lethal pathogenic process.) At the same time practically no studies on non-viral causes of AIDS-defining illnesses and on therapies to restore cellular immunity can be carried out.
The ideology that AIDS is caused by the so-called. HIV-retroviruses hides the fact that the illnesses constituting the AIDS-syndrome are caused mainly by malnutrition, dirty water and the poor living conditions in the countries of the developing world, the misuse of antibiotics and frequent consumation of oxidative drugs. The poor living conditions in the countries of the developing world are the result of a system of world trade, that allowes western countries to pay very low prices for raw materials, oil and food and to generate high profits from the credits given to poor countries.
Paralell to the World AIDS Conference (from 7th to 12th July in Barcelone) a conference of independent scientists, medical doctors, groups and activists from various countries, has debated at the Conference for Life (5th – 14th July in Barcelone) on the real causes of AIDS defining illnesses, the effects of non-toxic therapies for AIDS defining illnesses and on the social and political mesures to overcome AIDS. Partcipants of this congress and the acts organised for AMC (Madrid) have been: Heinrich Kremer (MD, Germany) Roberto Giraldo (MD, New York), Etienne de Harven (microbiologist, France), Mohammed Al-Bayati (toxicologist, USA), Christine Maggiore (Alive and well, USA), Gaetano Martino (MD, Italy), Manuel Garrido (MD, Spain) and groups from Columbia and Brasil and many more. Information on the lectures and discussions and on the conclusions made at this congress are available from: firstname.lastname@example.org
We think, that the question wheather AIDS defining illnesses are caused by transmittable pathogenic parts of the DNA in the cell nucleus (so-called HIV retroviruses) or by epigentic factors (malnutrition, dirty water, frequent infections, chemo-antibiotics and oxidative drugs) that induce a higher cell decay, a higher rate of reverse transcription, a higher rate of polyspecific antibodies (positive HIV-antibody-test) and the formation of cell particles of a certain morphology (so-called HIV-particles) has to get a clear answer.
Furthermore we have to ask, if the force administration of the toxic drugs (nucleoside analog substances and synthetic protease inhibitors) to suppress the formation of such cell-particles conforms to medical ethics. We consider this questions as important in regard of the administration of toxic genetic treatments to persons with chronic diseases, marked as carriers of pathogenic dispositions (parts of the DNA) by tests that dedect the morphology of cell particles. We also have to ask if the administration of the so-called HIV-vaccines, made of nacked DNA, to symptom-free persons with a negative test result conforms to medical ethics.
Felix de Fries
Study group AIDS therapy
Enclosure: Heinrich Kremer: Did Gallo and his collegues manipulate the HIV antibody test to order
DID DR. GALLO AND HIS COLLEAGUES MANIPULATE THE “AIDS-TEST” TO ORDER ?
“The hunt for the virus” 1 has degenerated into “clean torture with fatal result” 2
By Heinrich Kremer
Continuum Summer 1998
Who, for given reasons given below casts doubt on the theory that “HIV causes AIDS”, is often confronted with the question, if it did not, how is it that a patient who has been diagnosed as “HIV positive” by the test sooner or later goes on to develop
AIDS? To which the AIDS sceptic usually replies that a”HIV-positive” laboratory result, an arbitrary defined characteristic is part of the clinical diagnosis “AIDS”.
This exchange does not advance the argument very much as to whether “AIDS” and “HIV” are scientifically-speaking biologicalentities and if between them a biological cause-effect relationship is possible. In other words, if either the term “AIDS” or the term “HIV”, or neither, represents conceptually independent entities but rather purely semantic constructs, then biologically there can be no cause-and-effect relationship between these two terms, i.e. between the postulated pathogen “HIV” and the supposed definable disease entity “AIDS”.
The causative factor, the “retrovirus HTLV-III” (later termed “HIV”) was introduced by Robert Gallo in 1984 (then a retrovirologist in the Tumour Biology Laboratory in the National Cancer Institute at Bethesda).
On May 4, 1984 together with collaborators from his own laboratory and other research centres and hospitals as well as workers at the pharmaceutical company Litton Bionetics, he published four basic papers in Science (3-6). These supposedly described the identification, isolation and continuous production of a newly discovered type of retrovirus (since 1987 called “HIV”) as well as the serological analysis of this “HIV” and of tests “capable of detecting antibodies to HIV” in the sera of “patients with AIDS or pre-AIDS”. The simultaneous publication of these four papers by Gallo et al was shortly preceded by a patent application for “HIV antibody tests” and by Reagan’s US Health Secretary’sannouncement at a press conference attended by Robert Gallo himself before the world’s media that Robert Gallo and his team had “discovered the probable cause of AIDS”.
The first Science paper of May 4, 1984 begins with the fundamental assumption: “epidemiological data suggest that the acquired immunodeficiency syndrome (AIDS) is caused by an infectious agent that is horizontally transmitted by intimate contact or blood products” (3). The word ‘probably’ employed by the US minister only a few days before was no longer mentioned by Gallo et al.
The fourth and last Science paper of that date ends with theconclusion: “The data presented here and in the accompanyingreports suggest that HTLV-III is the primary cause of AIDS” (6). (HTLV-III = HIV). Gallo et al’s conclusion proves that they did
not postulate a direct cause-and-effect relationship betweenHIV” and “AIDS”, declaring “HIV” to be only the primary causeof “AIDS”: “Although the disease is manifested by opportunistic infections, predominantly Pneumocystis Carinii Pneumonia, and byKaposi’s Sarcoma, the underlying disorder affects the patient’s cell-mediated immunity, resulting in absolute lymphopenia and reduced subpopulation of helper T lymphocytes (OKT4+)” (3).
Gallo et al by no means, therefore, postulated that “HIV” was the direct cause of “AIDS”, rather, they only claimed “HIV” is the cause of “AID” (AID = Acquired Immuno Deficiency = reduced sub-population of T-helper lymphocytes).
The syndrome “S” (“manifested by opportunistic infections (OI), mainly Pneumocystis Carinii Pneumonia (= PCP), and Kaposi’s Sarcoma (=KS)”) was presented by Gallo et al like commonplace as the necessary consequence of “AID”.
The scheme of Gallo et al is as follows:
1. “HIV” causes “AID” as a consequence of the infection and sooner or later the destruction of T-helper lymphocytes.
2. As a consequence of the decrease of cellular immunity, the ontrol of opportunistic pathogens and cancer cells by T-helper
lymphocytes breaks down as a result of which, syndrome “S”develops.
The short version of Gallo et al’s plague formula is “HIV = AIDS”.
The two part causal chain “HIV causes AIDS” actually turns out to consist of three parts, and Gallo et al’s claim that “HTLV-III” (= “HIV”) is the primary cause of “AIDS” (6) is a fusion of two hypothetical causal assertions, and a fictitious end-effect assertion. This is because Gallo et al’s publishe data say nothing about whether “AID” really does cause “S”; they can at most suggest a cause-and-effect relationship between “HIV” and “AID”. Whether “S” can be the result of “AID” is for several reasons highly doubtful. “S” is somewhat chameleon-like due to numerous re-definitions undergone, so that the existence of “S” as a “separate disease entity” (4), in the sense of a biological disease entity, can no longer be rationally made out.
Individual, defined diseases, which initially made up part of the syndrome were years later expressly removed again. In the end a wild collection of 29 old infections and non-infectious diseases has been collected together to constitute the syndrome “S”, of which several are part of “S” even if the “HIV” status is negative or indeterminate (7).
The latter means that “AID” cannot be the cause of “S” because “AID” is supposed to be the result of “HIV”, in order that Gallo et al’s plague formula “HIV = AID = S” as a causal chain is upheld, yet “AID” due to different reasons can exist independently of “HIV”. Nothing is given whereby “AID” must be the cause of “S”. “AID” and “S” could, instead, have a common cause which need have no causal relationship with a hypothetical “retrovirus HIV”.
The pretence of a pseudo-biological cause-and-effect relationship expressed by the plague formula “HIV = AID = S” has made a leading AIDS critic, who has presented the most comprehensive clinical analysis of the AIDS phenomenon, say”AIDS, in short, has become a schizophrenic disease” (8).
How then, can a semantic construct of a collection of mostly contradictory diseases be the result of a supposed biological causal chain, which itself in turn is made up of hypothetical constructs as cause-and-effect factors? Because the premises and conclusions (3,6) which underlie Gallo et al’s plague formula can be falsified convincingly.Gallo et al have claimed that “epidemiological data prove that an infectious agent (3) is the cause of “AID”, and “AID” is the cause of “S”.” Essentially, Gallo et al arrived at this conclusion from the findings of the CDC that “S” (“OI, mainly PCP, and KS”) is significantly connected with very frequent promiscuity and predominantly receptive anal intercourse in homosexual men in the metropolitan areas in the US (3). However, this conclusion only demonstrates the arbitrary and selective interpretation of the clinical data by the CDC and Gallo et al. Highly promiscuous and predominantly receptive (unprotected) course arespecifically indicators simultaneously for infectious and non-infectious causal factors for “S” (“OI, mainly PCP, and KS”) as well as “AID” (decline in T-helper mphocytes in blood serum). The conclusion of a new infectious pathogen and simultaneous exclusion of all non-infectious causal factors is by no means compelling, although it determines to this day the theory that “HIV causes AIDS”.
Highly promiscuous behaviour and predominant receptive anal intercourse closely correlate with consumption of sexual stimulants, above all amyl and isobutyl nitrites. 95% of homosexual men in the US report regular use of nitrite (9,10).
Nitrite inhalation relaxes the smooth anal muscles, raises blood flow to the penis, raises pain threshold, heightens orgasm and unleashes a mild state of intoxication in the brain. Nitrite use predominantly but not exclusively became known in homosexual sex partners, and has been approaching ubiquitous in surveyed homosexual men in Western countries since the mid-70s (11,13).
High frequency promiscuity and predominantly receptive anal intercourse very often entails concomitant increased multi-infectivity and provocation of administrating antimicrobials, chemotherapy, antibiotics, antiparasitica, antimycotica, virusstatica and corticosteroids (14). The first by the CDC in June 1981 of five diseased homosexual men being treated for PCP contains some clinical information of their medical history and medication, because at the time, the all-encompassing description AIDS, masking the real symptoms, had not yet become entrenched: The five homosexual patients had not had sexual relations between themselves. All of the fivepatients used nitrites, and all five had been treated with TMP/SMX (TMP = trimethoprim, SMX = sulfamethoxazole) (15).
The substance TMP/SMX, also known as bactrim and septrin were introduced in the early 70s as a double chemotherapeutical folic cid inhibitor. Nitrite and SMX (a sulphonamide derivative) arestrongly electrophilic oxidising agents. Both oxidise ferrous iron in haemoglobin to ferric, and thereby reduce oxygen-binding capacity of red blood cells. This causes methaemoglobulinaemia (16,20), a progressively life-threatening deficiency in oxygen supply into the respiration chain of the mitochondria. The latter are former bacteria, which, as multifunctional organelles, supply energy to the whole cell in form of adenosine triphosphate (ATP) produced in oxidative phosphorylation (21).
Oxygen-dependent ATP synthesis and its resulting oxygen metabolites control the cell division cycle.
If too little oxygen is transported to the respiratory chain, the ratio of oxidative ATP production in the respiration chain (normally about 90%) may become inverted in favour of the non-oxidative ATP production (normally about 10%). Latest experimental findings suggest that the redox balance controls the genetic expression of proteins for the enzymes of the non-oxidative ATP production (glycolysis) (22).
Under normal physiological conditions, there is a rhythm of phase-linked change between oxidative energy production in the mitochondria and the change to non-oxidative glycolysis during the late stage of cell division (the S-phase of mitosis). If, through lack of oxygen under conditions of methaemoglobulinaemia, the genetic expression of glycolytic enzymes is not sufficiently inhibited (23), the cell may, despite intact mitochondria, and the presence of residual molecular oxygen, switch to permanent non-oxidative glycolysis and cationic load reversal.
This results in unrestrained cell division, which may ultimately lead to transformation to a tumour cell.
Along the oxygen transport route in the bloodstream, conditions in the most minute capillaries with a diameter below 100 nanometres, because of altered partial pressure of oxygen, are particularly favourable for the oxidation of the red haemoglobin, which can only bind oxygen when being in reduced form. Through diffusion and association to essential fatty acids through transit routes of the basic-tissues it can deliver oxygen to individual cells.
The mechanism of unrestrained activation of cell division (hyperplasia) in methaemoglobulinaemia, may, therefore, following hypoxaemic stress, above all in the smallest capillaries, affect the cells of the walls, – the endothelial cells. These endothelial cells are in direct contact with the hypoxaemic red blood cells. If hyperplastic conversion of endothelial cells occurs, that is called Kaposi’s Sarcoma. On the other hand, especially in rapidly dividing cells such as in thymus-matured precursor cells of T-helper lymphocytes, ATP production can decline to a critical value, if oxygen turnover is reduced permanently even by a small amount. This is a control mechanism, which in turn may affect the rate of mitosis. This interaction of haemoglobin oxidation by nitrites and antimicrobial drugs with oxidative phosphorylation may, in a situation of increased simultaneous consumption of T-helper lymphocytes as a result of slowing maturation of T-helper lymphocytes, be in part a cause of “AID”.
This chain of causal events is also supported by the”frightening possibility” (24) that nitrites may turn most classes of antibiotics into carcinogens (25). Excessive antibiotic consumption (whether prescribed or not; in a study 40% of male homosexuals admitted preventive use (26)) in conjunction with nitrites is a frequently encountered pattern of behaviour among male homosexuals especially in the large urban areas in Western countries (27).
Hypoxaemic stress can, therefore, explain the contradiction of simultaneous appearance of malignant hyperplasias (KS, lymphomas) and opportunistic infections, mainly PCP, in homosexual men (approx. 2/3 of “AIDS cases” in Western countries, excluding covered homosexual “AIDS patients” estimated by orthodox “AIDS”-doctors to amount to 50% of so-called heterosexual risk groups (28)), without ever introducing a hypothetical “retroviral” cause to explain the pathophysiology.
In contrast to this clear finding, Gallo et al tried to resolve the clinical contradiction between OI and KS by constructing a new “retrovirus HIV”. Gallo et al’s so-called retroviruses “HTLV-I” and “HTLV-II” are said to cause rare forms of leukaemia, i.e. cancers of the white blood cells, whereas “HTLV-III” (=”HIV”) is said to kill T-helper lymphocytes.
This concept has completely failed. The cytopathic effects of “HIV” demonstrated by Gallo et al have turned out to be laboratory artefacts (29). Gallo et al’s claim that “HIV” kills T-helper lymphocytes could, despite changing the theories, not be confirmed (30-33).
The disease theory “HIV causes AIDS” is itself based on several serious clinical misconceptions:
1. The agent causing PCP is not as Gallo claimed a protozoon.
The aetiology according to which after the destruction of T-helper lymphocytes by “HIV-infection”, Carinii pneumocytes, the cause of PCP, could escape control by T-helper lymphocytes and multiply unrestrictedly, is objectively wrong. Such protozoa simply do not exist (34,35).
What is involved are micro-fungi that are inhaled in the air, and which, for example, in the case of increased cell decay following hypoxaemic metabolic changes (including “AIDS” without “HIV”), find fertile terrain in the alveoli of the lungs. In this way, a harmless fungus (saprophyte) becomes the dangerous cause of PCP.
2. Contrary to what Gallo et al claimed, T-helper lymphocytes do not suppress the growth of cancer cells, because cancer cells do not have antigens through which T-helper lymphocytes could identify them (36). This means that the hypothetical destructionof T-helper lymphocytes by “HIV” and the ensuing disappearanceof the suppression of KS cells cannot be the cause of KS. The predicted increase of all other types of carcinoma in “AIDSpatients” resulting from the disappearance of the surveillance of cancer cells after the postulated destruction of T-helper lymphocytes by “HIV-infection” did not occur (37).
3. Contrary to the assumption of the CDC and Gallo, the hypothetical “HIV infection” of T-helper lymphocytes despite the postulated essentially alarm function of T-helper lymphocytes also for antibody production by B-plasma cells did not result in destroying defence capacity against all microbes. Unlike patients with impaired immune functions, E.G. intensive care patients in whom mortality following typical bacterial infections is up to 80%, strikingly in the “immune deficiency syndrome AIDS”, bacterial infections are rarely seen. The CDC under the category “AIDS indicator diseases” states explicitly for “bacterial infections, frequent or repeated”: “not applicable as indicator of AIDS in adults/adolescents” (37).
4. A fundamental pillar of the disease theory of Gallo et al according to which “HIV causes AIDS”, is severely dented by the actual epidemiological situation over the 15 years 1982-1997.
For example, in 1997 the German “AIDS Centre” registered 2736 KScases in total with 2505 KS cases in the category “homosexuals”. The remaining KS cases were in “heterosexual risk groups” or “no information on risk group”. On average, therefore, there were 15 KS cases a year, which were not primarily classified as “homosexual”. Because homosexual intravenous drug users are classified as intravenous drug users and at least 50% of the patients classified as “heterosexual men” and “not known” were subsequently reclassified as homosexuals (28,38), this is of the order of magnitude to be expected for KS cases classified as “non-homosexual men”. Corresponding epidemiological data for the prevalence of KS are available for other Western countries (39).
Gallo et al’s formulation “HIV = AID = S” is not, therefore, found to be true. “AID” (measurable decline in lymphocyte population in the blood, especially T-helper lymphocytes) though it can occur, in all members of “high-risk groups”, is evidently not the cause of “S” (“OI, mainly PCP, and KS”) because “S” can, first, occur without “AID” (29), and secondly, the combination of “S” (with KS) should, if the theory were correct, not exclusively be limited to homosexual patients. If, therefore, “S” is not necessarily the result of “AID”, what then is the common pathogenic indicator of “AID” patients as defined by Gallo et al to be “high-risk groups” (4)?
The common factor of “AID” patients (without necessarily resulting in “S”) is obviously the unusually high uptake of strongly oxidising substances (mitogens), and the huge variety of exogenous extraneous cells such as red blood cells, activated lymphocytes or sperm cells from individuals (allogenic stimulation (29,40)). It is beyond doubt that this oxidative stress (i.e. pro-oxidative vs. anti-oxidative metabolism) of “high-risk groups”, can overload the detoxification capacity and waste disposal capacity of the body which is furthermore supported by the finding that asymptomatic “HIV positives” belonging to “high-risk groups” show a strong shift from reduced to oxidised glutathione (41).
The glutathione system is essential for the removal of oxygen free-radicals, especially in the mitochondria (42,43). The oxidation of the central molecule of glutathione, cysteine, to cystine, in a chain reaction reduces the build up of glutathione and accelerates the destruction. It follows that the systemic decline of glutathione concentration in HIV positives can be due to both reasons, because of decreased synthesis and increased disposal.
“The oxidative stress to which AIDS patients are subjected would lead to cellular anomalies in many cells, including lymphocytes, resulting in opportunistic infection, immunological abnormalities and neoplasia” (44).
Does this finding of the overload of redox potentials in members of “high-risk groups” mean that “HIV”, too, or rather the “anti-HIV antibodies” are the result of oxidative bombardment on the cell-mediated immunity of the “high-risk groups”?
A specific load value of the diminution of the reduction force in the body of members of “high-risk groups” is hepatitis type B, in particular, in the chronically active form (45).
Gallo et al postulated in the first paragraph of the first publications in Science of May 4 1984 (except for the first rebutted premise: “Epidemiological data suggest that the acquired immunodeficiency syndrome (AIDS) is caused by an infectious agent” and the second (rebutted) premise: “AID” necessarily leads to “S”), a third premise: “Although patients with AIDS or pre-AIDS are often chronically infected with cytomegalo virus or hepatitis B virus, for various reasons these appear to be opportunistic or coincidental infections” (3).
This claim stands the clinical history completely on its head. “High-risk groups”, in Gallo’s definition “homosexual men with multiple sex partners, intravenous drug missusers, haemophiliacs, blood transfusion recipients and close heterosexual contacts of members of these high-risk groups” (6) were long before the so-called ‘sudden’ arrival of “HIV” (1978), recognised to be the most severely hepatitis-B affected groups of patients (46-50).
Hepatitis inducers (nowadays thought to be hepatitis-B, hepatitis-C) “appear to be thousands of times as infectious in clinical settings as HIV and represents a much more prevalent medical problem” (51). Hepatitis-B due to various patho-physiological reasons, especially in the chronically active form contributes significantly to oxidative stress, by restricting waste disposal and detoxification, and overloading of redox potentials. The body tries to compensate for this by increasing cortisol production. When this ultimately fails, hypercorticolism persists in a damaging way. A hypercatabolic metabolism results from this (i.e. excess cell decay vs. build up) (52). Cortisol as “synergiser” for a number of hormones and mediators effects activation of cyclic adenosine monophosphate (cAMP) and a displacement of the cAMP/cGMP ratio as principal indicator for increased cell turnover (53). The net effect is a dampening of cellular immunity and activation of humoral immunity. Resulting from the increased cell turnover, the decreased disposal of cell debris (because of the dampened cellular immunity, “AID”) and the strengthened autoimmune activity, a significantly increased formation of autoantibodies occurs which above all specifically bind to cytoskeletal proteins and extra-cellular proteins of the cell matrix asantigens (54, 33).
Concluding, it is fair to assume that Gallo et al took these attributes (25) of “high-risk groups” into consideration, namely,
1. the excessive oxidative (mitogenic) stress
2. allogenic stimulation by foreign cell components
3. the sharply increased antigen auto-antibody load together with suppression of T-cell dependent immunity brought about by synergistic effects of persistent corticolism with resulting change in cAMP/cGMP ratio.
In their original paper (“Detection, isolation and continuos production ..” (3)), Gallo et al were only able to cite indirect phenomena, such as reverse transcription, ultra-thin layer electron micrographs, banding of protein mixtures at given densities, which according to the established rules of virology are not acceptable as evidence for the existence of a virus or less a “retrovirus”, because these indirect phenomena can also be obtained in the absence of any viral entity under certain cell culture conditions (55-60,33).
Then the question becomes increasingly pressing: how did Gallo et al manage to produce a protein mixture in cell cultures and in the test tube, which as the substrate in the “AIDS-test” when in contact with serum of people in “high-risk groups”, resulted in a given rate of antigen antibody-reaction for single proteins (6) ?
Gallo’s papers, though written in highly technical language do not reveal this secret of test-constructing.
Only in 1987 when the disease theory “HIV causes AIDS” led to the introduction of a highly toxic DNA chain terminator (azidothymidine = AZT = Retrovir), was some light shed on this matter when two of Gallo’s former collaborators and co-authors of the original publications in Science of May 4 1984 (3-6) revealed the essential details. Mangalasseril Sarngadharan and Phillip Markham (collaborators of Litton Bionetics, Kensington MD, USA) published the biochemical methods used by Gallo et al whereby they manipulated the protein mixture, which due to self-defined conventions are said to be “HIV antigens” (59).
To start with, Gallo et al biochemically prepared cell components obtained from members of “high-risk groups” according to the self-defined rules of “retrovirus production”. This procedure only “from time to time” and only transiently (61) led to the production of unspecific phenomena as surrogates for the existence of a new “retrovirus”. Then they mixed lymphocytes from patients in “high-risk groups” with exceptionally rapidly dividing leukaemia cells (3,4). This cell mixture was then subjected to the effects of certain biochemical substances.
They go on to say that “in vitro stimulation was achieved by mitogens or added cells (allogenic antigens ) …
Certain manipulation of culture conditions improved the result, for example, co-cultivation of patients’ cells with peripheral white blood cells, which were stimulated by mitogens, from non-infected donors.
The “virus isolation” of cultured cells was also significantly facilitated by adding hydrocortisone to the culture medium” (61).
Knowing the specific antigen auto-antibody status of “high-risk groups” patients, it is possible, therefore, to trigger, on demand, an antigen mixture appropriate to the auto-antibody repertoire in serum from high-risk patients, in cell cultures of human lymphocytes, co-cultured with leukaemic cells when subjected to specific biochemical manipulation.
The apparent proof that in the antigen mixture one is dealing with “retroviral” proteins, brought about by the demonstration of a naturally occurring repair mechanism – reverse transcriptases, produced particularly copiously in cancer cell cultures to repair DNA and renew chromosome ends, hence co-cultivation with leukaemic cells in Gallo et al cell culture (3,4), as well as proof of exocytotic virus-like particles (frequently occurring transport particles to expel intra-cellular components from mitogenically stimulated cells) as proof of “isolation and continuous production” of supposed retroviruses is misinterpretation (33).
That Gallo et al’s sensational discovery of a “new retrovirus” was in fact a laboratory artefact is made explicit by Gallo et al’s expressly stating that “HTLV-I” (isolated from T-cells in 10% of “AIDS patients”) and “HTLV-II” from the “family of retroviruses” in “AIDS patients”, were also discovered and demonstrated (3,4). Later on, there was no further mention of “HTLV-I” and “HTLV-II” being “isolated from T-cells of AIDS patients”. Nor were there noticeable occurrences of leukaemia in “AIDS patients”. The “isolation” of “HTLV-I” and “HTLV-II” was a laboratory artefact due to the rules of “retrovirus-production” of Gallo et al. By analogy this finding accounts for “HTLV-III” (= “HIV”) as well.
In effect, therefore, Gallo et al were adapting conditions which they knew to be conducive to antigen formation in the body of”high-risk patients”, to laboratory conditions. The difference is that in cell culture as opposed to the body of “high-risk patients”, no antibodies are present because the B-plasma cells are absent. Then it is possible, at a certain arbitrarily fixed auto-antibody level, to demonstrate an antigen-antibody reaction when the antigen mixture of the cell culture is brought in contact with sera of “high-risk patients”. This is exactly the principle employed in “anti-HIV-antibody tests”. In mirror image fashion, the artificially produced antigens bind to the auto-antibodies, whose presence was to be expected because of the well-known pathophysiological overload of “high-risk patients”.
In describing the recipes of Gallo et al’s, who covered their laboratory-tricks behind the dust screen of patents, the irrational reduction of “AID” to the effect of a seemingly new infectious cause (3) and the ignoring of the clinical effect of chronic hepatitis (3) becomes apparent: as a claim used to create pressure to introduce the patented “antibody test system” of a “new retrovirus” found in the National Institute of Cancer.
The laboratory finding of “HIV positive” which may be diagnosed in those belonging to “high-risk groups” depending on the quantity and personal reaction pattern of antibodies, may also be made in rare cases in those not belonging to “high-risk groups” for a number of extremely diverse reasons.
Gallo et al’s expectations regarding the dynamics of the spread of “HIV” have, contrary to the horrendous predictions, not been fulfilled in the real biological world. In Germany, for example, according to official figures for the 15 years 1982-97, out of a population of 82 million, 60.000 have been notified as HIV positive, i.e. more than 99.9% of the population are personally not affected by “HIV” and “AIDS”. The official government forecasts, until now uncontradicted, spoke of there being more “AIDS cases” by 1996 than there were inhabitants.
At least every other person was supposed to have died by 1996, unless a vaccine or drug against the “absolutely” fatal plague had become available (60). In the former East Germany, there have been a grand total of 252 cases in a population of 16 million, and that despite massive migrations (since the fall of the wall) up to the end of 1996. Over the past decade in the whole of Germany there has been a very constant 2-3.000 number of people diagnosed annually as HIV positive. 95 % of these have been classified as belonging to the “high-risk groups” of “homosexual men” and “IV-drug user” (homosexual IV-drug users are counted as ordinary IV-drug users). 5% of “HIV positives” are considered to be false positives, but cannot be identified as such by the test.
At most 2000 “HIV positives” develop AIDS annually, and 1300 patients die annually of “AIDS” (actual cause of death is not revealed). Of the supposed 60.000 HIV positives (figures are very unreliable because of unknown multiple reporting), 50.000 are still officially alive today. 54% of all “AIDS patients” gave their addresses to be one of the six largest cities, in which 10% of the general population also live. Opposed to that in 90% of the remaining inhabitants only 44% of the notified “AIDS cases” occur.
For example the disease rate and death rate of “HIV-positive” haemopholiacs registered in these six cities is twice as high as in “HIV-positive” haemophiliacs living outside of those cities.
In these cities (Berlin, Hamburg, Köln, Düsseldorf, Frankfurt and München) the university clinical “AIDS-treatment centres” are located which report the highest “AIDS”-disease- and death-rates to the national AIDS-centre.
As the positions of collaborators the “AIDS-ambulances” and “AIDS-stations” of these university clinics mostly are paid by the pharmaceutical companies, the connection between Medicine and market (“AIDS-test”, “AIDS”-medications”) becomes all too obvious. Very intriguing is the comparison between the “capitalist” West-Berlin and the former “socialist” East-Berlin.
In the period of 15 years from 1.1.1982 to the 1.1.1997 in West-Berlin (2,2 million inhabitants, which make less then 3% of Germany’s population) 3083 “AIDS-cases” have been registered which are 20% of all German “AIDS-cases”. In the same period (including 7 years of unification with West-Berlin after the fall of the Berlin wall 1989) in East-Berlin (1,3 million inhabitants = 1,6% of the German population) only 152 “AIDS-cases” are registered, which make 1% of all German “AIDS-cases”. This very intriguing, by chance historical and model-like data (38) proofs wrong the premise of Gallo et al. that “epidemiologic data suggest that the acquired immunedeficiency syndrome (AIDS) is caused by an infectious agent”. The disease rate when brought in connection with the whole population is obviously a very rare medical event, not dependent on a ubiquitous transmittable mass-virus, but determined by life-style in a largely commercialised subculture and/or by uncritical medical intervention in Western society of super-abundance.
Or pathophysiologically spoken: “AIDS-patients” come down due to a lack of power of reduction (caused by superoxidation and /or hypoxaemia) in the midst of a redundant medical over-supply.
To argue against Gallo et al. refers to Africa, which is uncritically presented by mass-media as the “dying AIDS-continent”. Too, in this context the world of facts seemingly is overwhelmed by a virtual, only imagined world of information.
In Africa south of the Sahara, the annual increase in population was about 100 million inhabitants over the last decade, even though the latest report on the world population states, that according to a lot of population experts “in the third world the plague supported the birth-planing more than any earlier programs” (63). Due to the lacking medical infrastructure and low budgets in the health care system (in most states south of Sahara the average annual spending per head of the population for providing health care is 6 US$, a single complete “AIDS-test” – 2x ELISA-test, 1x Westernblot – costs much more than 6 US$) the “AIDS-test” is not widely used. Instead of this the World Health Organisation (WHO) transfers certain amounts of money to the health authorities of the various countries for “AIDS-education” in order to get estimated incidental rates of “HIV-infection” and “AIDS-cases” which are not verified by the WHO.
WHO-experts use these estimates in calculations based on the supposed “dynamic of distribution” of the “HIV-plaque” and present the resulting numbers to the world media as “HIV-infection” and “AIDS-disease” in Africa. Usually, in the subsequent media reports the speculative “HIV-infections” and “AIDS-diseases” are lump-summed and wrongly reported as “AIDS-cases” in Africa. This is the way the manipulated numbers of more than 20 million “AIDS-cases” in Africa (app. 90% of the world-wide reported “AIDS-cases”) came into existence without any substantial base of knowledge (64).
The fictious loom scene of a “people murdering AIDS-plaque” in the “global media village” acted again enhancing on the selling of “AIDS-tests” and “Anti-HIV-medications” (euphemicly termed “cocktail-therapy”) in western countries, in a way that “poor Africa” unwillingly was misused to increase sales in the “rich West”.
The data on the clinical, immunological, virological and epidemiological progress since 1984 show beyond any doubt that the disease-theory “HIV causes AIDS” has no concurrence with the biological reality. As a marketing strategy Gallo’s manipulated “AIDS-test” has been extremely successful. But this at the cost of the health and life of uncounted children, women and men who, from a medical ethic point of view became victim to “clean torture with case of death” induced by the arbitrary medical death-sentence of a “HIV-positive” result. Medical ethical behaviour “according to best wisdom and conscience” must signify to make, out of your own, the effort to inform yourself on the basis of existing data about possible manipulations in diagnostic and therapy and to use the given alternative therapies instead of inducing fear blind with rage (33). *
Address of the author: – Dr. med Heinrich Kremer – Metzendorfer Weg 36 – D 2122 Rosengarten (b. Hamburg)
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“Il paziente malato di Aids NON muore a causa del virus dell’HIV ma per alterazioni dell’assorbimento intestinale e quindi per ipoalimentazione (malNutrizione), dovuta a una grave micosi.” (By Dott. Gerhard Orth, Leuthkirch)
RETHINKING AIDS IN AFRICA UNDER DEVELOPMENT & RACIAL STEREOTYPES
By Charles L. Geshekter – Reappraising AIDS Sept./Oct. 1997
The problem with the truth is that it is mainly uncomfortable and often dull . — H.L. Mencken
Millions of Africans have long suffered from severe weight loss, chronic diarrhea, fever, and persistent coughs.
In 1985 Western researchers suddenly defined this cluster of symptoms as a distinct syndrome, AIDS, and declared that it was caused by a single virus, HIV, which they considered to be sexually contagious.(1)
American health officials universally accept this HIV-AIDS model to explain what used to be considered the diseases of rampant poverty in Africa. There are at least three reasons why this view needs careful reconsideration.
First is the fact that many of the Africans who qualify for AIDS diagnoses — perhaps as many as 70% — turn out to be negative when tested for HIV.
Second is the failure of the African HIV-AIDS model to predict the course of AIDS in the United States.
Since AIDS symptoms are widespread in the general African population,(2) if it transmits heterosexually it should also become widespread in other general populations, such as Americans, in which hundreds of thousands of heterosexuals annually contract venereal diseases. Instead, 16 years after it was first described in the medical literature, in the United States AIDS has remained rigidly confined to special risk groups. Of the 70,000 annual American AIDS patients, at least 90% are drug users (including nearly all the gay patients), and fewer than 10,000 are designated as heterosexual cases.
Third, sexual transmission can’t explain the differences in rates of HIV positivity between African (about five per 100) and American (about one per 7,000) heterosexuals. When the HIV-AIDS paradigm made its debut in 1984, its proponents assumed that HIV was easily transmitted coitally. Scientists tested this idea only years later, though, when they arrived at extremely low coital transmission frequencies. The latest study shows that an HIV-negative woman converts to positive on average only after one thousand unprotected
contacts with a positive man, and a negative man becomes positive on average only after eight thousand contacts with a positive woman.(3)
These data suggest two mutually exclusive conclusions. Either HIV isn’t a sexually transmitted microbe after all, and other factors account for HIV prevalence; or African heterosexuals are wildly more promiscuous than American heterosexuals, a scenario that surely is not true.
With all of this in mind, why do so many health professionals consider it useful or necessary to view the diseases of poverty in Africa as sexually contagious? And why did they ever believe it?
Defining AIDS in Africa
CDC physicians Joseph McCormick and Susan Fisher-Hoch convened the WHO conference in the Central African Republic in 1985 that produced the “Bangui Definition” of AIDS in Africa. The CDC had just adopted the HIV-AIDS model to explain the diseases of American drug injectors, a cohort of promiscuous urban gays in the party drug scene, and transfusion recipients. HIV turned out to be one of the many viruses that tended to react with blood from these patients. The same was true of blood from Africans afflicted with the diseases of poverty. The HIV-AIDS model assumed that AIDS would “spread” via HIV to a much larger fraction of Africans than those who currently suffered from it.
McCormick and Fisher-Hoch accepted this model. They recently explained their motivation for the conference and the rationale behind the AIDS definition that resulted from it:
We still had an urgent need to begin to estimate the size of the AIDS problem in Africa….But we had a peculiar problem with AIDS. Few AIDS cases in Africa receive any medical care at all. No diagnostic tests, suited to widespread use, yet existed…In the absence of any of these markers [e.g., diagnostic T4/T8 white cell tests], we needed a clinical case definition…a set of guidelines a clinician could follow in order to decide whether a certain person had AIDS or not. [If we] could get everyone at the WHO meeting in Bangui to agree on a single, simple definition of what an AIDS case was in Africa, then, imperfect as the definition might be, we could actually start to count the cases, and we would all be counting roughly the same thing. [emphasis added]
The definition was reached by consensus, based mostly on the delegates’ experience in treating AIDS patients. It has proven a useful tool in determining the extent of the AIDS epidemic in Africa, especially in areas where no testing is available. Its major components were prolonged fevers (for a month o more), weight loss of 10 percent or greater, an prolonged diarrhea.(4)
The doctors wanted to refute the ugly moralism of the 1980s that AIDS was a “gay plague” by convincing the American government that “AIDS was a plague all right, but that no one was immune.”(5)
McCormick and Fisher-Hoch recalled that:
experts in STDs continued to regale us with tales of the excessive and often bizarre sexual practice associated with HIV in the West… We were also beginning to see a direct correlation between the number of sexual partners and the rate of infection…Compared to the West, heterosexual contacts in Africa are
frequent, and relatively free of social constraints — at least for the men…. There was every reason to believe
that, having found heterosexually transmitted AIDS in Kinshasa, we were likely to find it everywhere else in
It was upon these grossly unscientific claims, inaccurate clinical generalizations, western notions of sexual morality, and 19th-century racist stereotypes about Africans that AIDS became a “disease by definition.” Africa was assigned a central role in promoting the premise that AIDS was everywhere and everyone was
at risk. By 1986, “people were falling over one another to get involved in AIDS research,” recalled the couple. “They realized that AIDS represented an opportunity for grant money, training, and the possibility of professional advancement… A certain bandwagon mentality took hold.
Careers and reputations were riding on the outcome.”(7)
As proof that these “AIDS symptoms” were sexually transmitted, McCormick and Fisher-Hoch point to a narrow survey conducted by Kevin DeCock, another CDC epidemiologist. In 1986, DeCock examined stored blood samples taken in 1976 (for Ebola virus testing) of 600 residents of the small town of
Yambuku, in northern Zaire. Samples from five patients (0.8%) tested positive for HIV antibodies.
DeCock wanted to know what happened to those five people during the intervening ten years. According to McCormick and Fisher-Hoch, “three of the five [60%] were dead. To determine if their deaths were attributable to AIDS, Kevin interviewed people who had known them. The friends and relatives of the
deceased described an illness marked by
severe weight loss and other ailments that left little doubt in Kevin’s
mind that they had succumbed to AIDS [emphases
DeCock concluded from these interviews that the dead subjects died from AIDS, and that HIV had caused it. He reached this conclusion without properly matching the five HIV-positive patients with peers from among the 595 HIV-negative subjects, and without collecting mortality data and morbidity information about them as well. Had he done this, perhaps he would have discovered that even HIV-negative Africans die of “severe weight loss” and other so-called AIDS conditions.
DeCock further noted that antibody tests conducted in 1986 showed that the HIV prevalence in Yambuku had remained constant at 0.8% during the ten years since 1976. As far has he was concerned, this meant that HIV — and thus AIDS — really did originate in Africa. HIV (AIDS) existed for years in small numbers of rural inhabitants (who had contracted the HIV from primates, he imagined). He speculated that once some of those people in the late ’70s migrated to what DeCock falsely assumed were sex-crazed cities, an epidemic of HIV and AIDS exploded.
DeCock did not consider that these same data could have been interpreted as indicating that HIV is a mild virus, and difficult to transmit. Neither did McCormick and Fisher-Hoch.
The sort of presumptive diagnosis employed by DeCock is known as a “verbal autopsy.” It is widely accepted in Africa, where “no country has a vital registration system that captures a sufficient number of deaths to provide meaningful death rates.”(9)
While medically certified information is available for less than 30% of the estimated 51 million deaths that occur each year worldwide, the Global Burden of Disease Study (GBD) found that sub-Saharan Africa had the greatest uncertainty for the causes of mortality and morbidity since its vital registration figures were the lowest of any region in the world — a microscopic 1.1% (10)
These findings prompted The Lancet to acknowledge editorially that “current strategies to improve the world’s health may need to be reassessed” and to ponder “how much more money is spent on research into HIV infection [the 30th cause of death] than into the causes of suicide [#12] or the prevention of road-traffic accidents [#9] and why should this be.”(11)
Racism and African Sexuality
Whereas AIDS in the industrialized countries almost exclusively confines itself to a tiny percentage of homosexuals, drug injectors, and transfusion patients, AIDS afflicts the same general African population that faces such ancient scourges as malaria, schistosomiasis, and sleeping sickness (trypanosomiasis).
This is known as the “heterosexual paradox” of AIDS. Champions of the HIV model attempt to explain it in two contradictory ways. Some simply declare that the paradox is temporary.
They speculate that HIV arrived first in Africa and, in time, AIDS will be just as rampant in the West. However, they’ve been saying this now for over ten years.
Others recognize the permanence of the paradox. They account for it by declaring that Africans are just different from Westerners. They are substantially more promiscuous and more likely to have genital ulcers. How else to explain the widespread distribution of a virus that requires, for non-ulcerated genitals, a thousand heterosexual acts?
At the 10th International AIDS Conference in Yokohama (August 1994), Dr. Yuichi Shiokawa claimed that AIDS would be brought under control only if Africans restrained their sexual cravings. Professor Nathan Clumeck of the Universite Libre in Brussels was skeptical that Africans will ever do so. In an interview with Le Monde , Clumeck claimed that “sex, love, and disease do not mean the same thing to Africans as they do to West Europeans [because] the notion of guilt doesn’t exist in the same way as it does in the Judeo Christian culture of the West.”(12)
Such racist myths about the sexual excesses of Africans are old indeed.
Early European travelers returned from the continent with tales of black men performing carnal feats with unbridled athleticism with black women who were themselves sexually insatiable. These affronts to Victorian
sensibilities were cited, alongside tribal conflicts and other “uncivilized” behavior, as justification for colonial social control.
AIDS researchers added new twists to an old repertoire: stories of Zairians who rub monkeys’ blood into cuts as an aphrodisiac, of ulcerated genitals, and of philandering East African truck drivers who get AIDS from prostitutes and then go home to infect their wives.(13)
A facetious letter in The Lancet even cited a passage from Lili Palmer’s memoirs as evidence for how a large male chimpanzee’s “anatomically unmistakable signs of its passion for [Johnny] Weismuller” on the Tarzan set in 1946 “may provide an explanation for the inter-species jump” of HIV infection.(14)
No one has ever shown that people in Rwanda, Uganda, Zaire, and Kenya — the so-called “AIDS belt” — are more active sexually than people in Nigeria, which has reported only 3,002 cumulative AIDS cases out of a population of 100 million, or Cameroon, which reported only 8,141 cases in 10 million. (15)
No continent-wide sex surveys have ever been carried out in Africa.
Nevertheless, conventional researchers perpetuate racist stereotypes about insatiable sexual appetites and carnal exotica.
They assume that AIDS cases in Africa are driven by a sexual promiscuity similar to what produced — in combination with recreational drugs, sexual stimulants, venereal disease, and over-use of antibiotics — the early epidemic of immunological dysfunction among a small sub-culture of gay men in the West.(16)
The research from Africa suggests nothing of the sort. In 1991 researchers from Medicins Sans Frontieres and the Harvard School of Public Health did a survey of sexual behavior in the Moyo district of northwest Uganda. Their findings revealed behavior that was generally not very different from that of the West. On average, women had their first sex at age 17, men at 19. Eighteen per cent of women and 50% of men
reported premarital sex; 1.6% of the women and 4.1% of the men had casual sex in the month preceding the study, while 2% of women and 15% of men did so in the preceding year. (17)
The media misrepresentations that link sexuality to AIDS have spawned inordinate anxieties and moral panics in regions of Africa already afflicted with extreme poverty, ravaged by war, and deprived of primary health care delivery systems.
The “disaster voyeurism” of tabloid journalism enables them to use AIDS to sell “more newspapers than any other disease in history. It is a sensational disease — with its elements of sex, blood and death it has proved irresistible to editors across the world.”(18)
Public health seems to require salesmanship, not skepticism. The media’s appetite for scary scenarios and its disdain for alternative perspectives enables it to treat Africa in apocalyptic terms. This marketing of anxiety helps to promote behavior modification programs to “save Africa.” Oblivious to the morbidity and mortality data from the Global Burden of Disease Study, journalists reflexively maintain that “AIDS is by far
the most serious threat to life in Africa.”(19)
The serious consequences of claiming that millions of Africans are threatened by infectious AIDS makes it politically acceptable to use the continent as a laboratory for vaccine trials and the distribution of toxic drugs of disputed effectiveness like ddI and AZT. On the other hand, campaigns that advocate monogamy or abstinence and ubiquitous media claims that “safe sex” is the only way to avoid AIDS inadvertently
scare Africans from visiting a public health clinic for fear of receiving a “fatal” AIDS diagnosis. Even Africans
“with treatable medical conditions (such as tuberculosis) who perceive themselves as having HIV infection fail to seek medical attention because they think that they have an untreatable disease.”(20)
Some Western scientists, including Dr. Luc Montagnier, the French virologist who discovered HIV, claim that the practice of female circumcision facilitates the spread of AIDS.(21)
Yet Djibouti, Somalia, Egypt, and Sudan, where female genital mutilation is the most widespread, are among the countries with the lowest incidence of AIDS.
Does the “AIDS epidemic” in Africa portend the future of the developed world? The scientific establishment certainly thinks so. Biomedical funds that had been earmarked to fight African malaria, tuberculosis, and leprosy are now diverted into sex counseling and condom distribution, while social scientists have shifted their attention to behavior modification programs and AIDS awareness surveys.
Good Intentions, Bad Science: HIV Tests and Disease
A reappraisal of AIDS in Africa must recognize that HIV tests are notoriously unreliable among African populations where antibodies against endemic conventional viruses and microbes cross-react to produce ludicrously high false-positive results. For instance, a 1994 study on central Africa reported that the microbes responsible for tuberculosis and leprosy were so prevalent that over 70% of the HIV-positive test results there are false.(22)
The study also showed that HIV antibody tests register positive in HIV-free people whose immune systems are compromised for a wide variety of reasons, including chronic parasitic infections and anemia brought on by malaria.
The very low frequency of vaginal transmission of HIV makes it hard to imagine that heterosexual transmission can be responsible for high rates of HIV prevalence observed in some regions.(23)
So what is responsible ?
Perhaps the tests used to determine HIV infection in Africa overstate the prevalence. Some HIV tests detect entities believed to be part of HIV itself, such as certain proteins or genetic sequences. But in Africa HIV prevalence is determined by testing for antibodies, which are components of the host immune system, not the virus. The fact that these tests react with antibodies triggered by ordinary African microbes suggests an explanation for HIV prevalence in Africa that is more plausible than sexual transmission. (24)
Even the association of HIV antibody tests with ordinary infections does not mean that positive results warrant a prognosis of death. Consider an investigation, reported in The Lancet , of 9,389 Ugandans with unequivocal HIV antibody test results.(25)
Two years after enrolling in the study, 3% had died, 13% had left the area, and 84% remained. There had been 198 deaths among the seronegative people and 89 deaths in the seropositive ones. Medical assessments made prior to death were available for 64 of the HIV-positive adults. Of these, five (8%)
had AIDS as defined by the WHO clinical case symptoms. The self-proclaimed “largest prospective study of its kind in sub-Saharan Africa” had tested nearly 9400 people in Uganda, the so-called epicenter of AIDS in Africa.
Yet of the 64 deaths recorded among those who tested positive for HIV antibodies, only five were diagnosed as AIDS-induced.
If it is not sexual transmission of HIV, then what causes the widespread appearance of AIDS symptoms throughout Africa? The evidence strongly implicates the ordinary, widespread socio-economic conditions that give rise to AIDS symptoms even among HIV-negative Africans.(26)
In her meticulous 1997 doctoral dissertation, Michelle Cochrane juxtaposed the central tenets of AIDS orthodoxy against the material record of San Francisco AIDS patients’ charts. She found that public health officials persistently over-estimated the risk of contracting HIV/AIDS through sexual activity, “while simultaneously under-estimating the proportion of the HIV/AIDS caseload that were attributable to
intravenous drug use and/or socio-economic factors which condition access to health care and prevention services.”(27)
Cochrane showed that health officials conspicuously failed to investigate all risk factors for immunological dysfunction among heterosexual adult females.In their surveillance studies, it was considered sufficient for a heterosexual female merely to claim that the source of her infection was sex with an IV-drug user or another man
at risk for HIV/AIDS… A percentage of the 187 female AIDS cases [out of 24,371 cumulative cases
in San Francisco] attributed to sexual transmission could, with proper investigation, be attributable to
IV-drug use. Epidemiological research in the United States and Europe has never proven that a female has sexually transmitted HIV to a man. [Because] heterosexual transmission of HIV from a male to a female happens with difficulty and very infrequently… all AIDS surveillance statistics on female AIDS cases have been gathered without rigorous scrutiny of the woman’s risk for disease and with a bias towards including as many women as possible [emphasis added].(28)
The a priori assumptions that directed AIDS surveillance activities in the United States subsequently allowed predictions about an exponential spread of the disease to survive as “common knowledge,” despite the lack of empirical data. These are critical points to consider when reviewing any epidemiological data
on “AIDS” cases in Africa.
For the period 1984-95, the WHO compared estimates of HIV seropositivity with the actual numbers of AIDS cases in its Weekly Epidemiological Reports. The cumulative result is that 99.95% of all Africans do not have AIDS — including 97% of those who test HIV-positive. These facts strikingly contradict the popular view of an Africa overrun by fatal HIV infections.(29)
AIDS and the Medicalization of Poverty
Primary health care systems in Africa will remain hampered until public health planners systematically gather statistics on morbidity and mortality to accurately show what causes sickness and death in specific African countries. During the past ten years, as the external financing of HIV-based AIDS programs inAfrica dramatically increased, money for studying other health problems remained static, even though deaths from malaria, tuberculosis, neo-natal tetanus, respiratory diseases, and diarrhea grew at alarming rates.(30)
While Western health leaders fixate on HIV, 52% of sub-Saharan Africans lack access to safe water, 62% lack proper sanitation, and an estimated 50 million pre-school children suffer from protein-calorie malnutrition.(31)
Poor harvests, rural poverty, migratory labor systems, urban crowding, ecological degradation, social mayhem, the collapse of state structures, and the sadistic violence of civil wars constitute the primary threats to African lives.(32)
When essential services for water, power, and transport break down, public sanitation deteriorates, and the risks of cholera, tuberculosis, dysentery, and respiratory infection increase.
WHO Director General Hiroshi Nakajima warns emphatically that “poverty is the world’s deadliest disease.
Indeed, the leading causes of immunodeficiency and the best predictors for clinical AIDS symptoms in Africa are impoverished living conditions, economic deprivation, and protein malnutrition, not extraordinary sexual behavior or antibodies against HIV, a virus that has proved difficult or impossible to isolate directly, even from AIDS patients.
The so-called “AIDS epidemic” in Africa has been used to justify the medicalization of sub-Saharan poverty. Thus, Western medical intervention takes the form of vaccine trials, drug testing, and almost evangelistic demands for behavior modification.
AIDS scientists and public health planners should recognize the role of malnutrition, poor sanitation, anemia, and ordinary infections in producing clinical AIDS symptoms in the absence of HIV.(34)
The data strongly suggest that socio-economic development, not sexual restraint, is the key to improving the health of Africans.
Medically trained charity workers Phillipe and Evelyn Krynen, employed by the French group Partage, in Kagera Province of Tanzania, report that when “appropriate treatment was given to villagers who became ill with complaints such as pneumonia and fungal infections that might have contributed to an AIDS diagnosis, they usually recovered.”(35)
A similar observation comes from Father Angelo D’Agostino, a former surgeon who founded Nyumbani, a hospice for abandoned and orphaned HIV-positive children in Kenya:
“People think a positive test means no hope, so the children are relegated to the back wards of hospitals
which have no resources and they die. They are very sick when they come to us. Usually they are depressed,
withdrawn, and silent… But as a result of their care here, they put on weight, recover from their infections, and thrive. Hygiene is excellent [and] nutrition is very good; they get vitamin supplements, cod liver oil, greens
every day, plenty of protein. They are really flourishing.”(36)
People can be encouraged to behave thoughtfully in their sexual lives if they are provided with reliable information about condom use, contraception, family planning, and venereal diseases.
Multilateral institutions and African AIDS educators should familiarize themselves with the scientific literature that demonstrates the contradictions, anomalies, and inconsistencies in the HIV/AIDS orthodoxy.(37)
They have a major responsibility to consider the non-contagious explanations for “AIDS” cases in Africa and to stop the proliferation of terrifying misinformation that equates sexuality with death. *
1 – Gilks CF “What use is a clinical case definition for AIDS in Africa?” BMJ 303:1189-90, (Nov. 9, 1991).
2 – Bentwich Z, “Immune activation is a dominant factor in the pathogenesis of African AIDS”, Immunology Today 16(4):187-91 (1995).
3 – Padian N “Heterosexual transmission of HIV” Am J Epidem 146:350-7 (Aug. 15, 1997).
4 – McCormick JB, Level 4: Virus Hunters of the CDC (Atlanta: Turner Publishing, 1996) pp. 188-90.
5 – Ibid ., 176.
6 – Ibid ., 173-74.
7 – Ibid ., 179-80.
8 – Ibid ., 193.
9 – Kitange HM, BMJ 312:216-17(Jan. 27, 1997).
10 – Murray C, The Lancet 349:1269-76 (May 3, 1997).
11 – Editorial, The Lancet 349 (May 3, 1997) 1263.
12 – Jau JY Le Monde section of Manchester Guardian Weekly (Dec. 14,1993).
13 – Conover T, “Trucking through the AIDS belt, ” The New Yorker (Aug. 16, 1993).
14 – Sebastian R, “Did AIDS start in the jungle?”, The Lancet 348:1392 (Nov. 16, 1996).
15 – WHO, Weekly Epidemiological Record 71(26):215 (July 1, 1996).
16 – Review of: Rotello G, Sexual Ecology: AIDS and the Destiny of Gay Men , (New York: Dutton, 1997); Signorile M Life Outside: The Signorile Report on Gay Men , (New York: Harper Collins, 1997); Kevles D “A Culture of Risk”, New York Times Book Review (May 25, 1997), p8; Sonnabend J, “Fact and Speculation about the cause of AIDS,” AIDS Forum 2(1):2-12; Lauritsen J, The AIDS War (New York: Asklepios Press, 1993).
17 – Schopper D, Social Science and Medicine 37(3):401-12, (Aug. 1993).
18 – Deane J, SIDAfrique 8/9:29 (1996).
19 – Commentary, The Economist , p38 (Sep. 7, 1996).
20 – Chintu C, The Lancet 349:649 (March 1, 1997).
21 – Bass T, Reinventing the Future (Reading, Massachusetts:Addison-Wesley, 1994).
22 – Kashala O, J Inf Diseases 169:296-304 (Feb. 1994).
23 – de Vicenza NEJM 331:341-46 (1994); and Mandelbrot L, The Lancet349:885-89 (March 22, 1997).
24 – Papadopulos-Eleopulos E, Bio/Technology 11:696-707 (June, 1997).
25 – Mulder DW, The Lancet 343:1021-23 (April 23, 1994).
26 – Papadopulos-Eleopulos E, W J Microbiology and Biotechnology 11:141-42 (March 1995).
27 – Cochrane M, “The social construction of knowledge on HIV and AIDS,” PhD dissertation, Department of Geography, UC-Berkeley (April 1997), p. 7.
28 – Ibid ., pp. 259-60.
29 – WHO, World Health Report 1996 , p130.
30 – WHO, Bridging the Gaps (Geneva: WHO, 1995), Table 5 and Table A3; WHO, World Health Report 1996, Table 4 and Table A3.
31 – The Lancet , p69 (Jan. 11, 1997).
32 – Murray C, The Global Burden of Disease (Cambridge: Harvard Univ. Press, 1996).
33 – WHO, The World Health Report 1995 .
34 – Geshekter C, Transition 67:4-14 (Fall 1995); Patton C, Inventing AIDS (New York: Routledge 1990).
35 – Hodgkinson N in Duesberg P, AIDS: Virus or Drug Induced ? (Dordrecht: Kluwer, 1996), p. 353.
36 – Ibid ., pp. 350-51.
37- Chirimuuta R, AIDS, Africa, and Racism (London: Free Association Press 1989); Root-Bernstein R, Rethinking AIDS (New York: Free Press 1993); Duesberg P, Infectious AIDS: Have We Been Misled ?
Berkeley: North Atlantic Books 1996); Brody S, Sex at Risk; Lifetime Number of Partners, Frequency of Intercourse and the Low AIDS Risk of Vaginal Intercourse , (New Brunswick: Transaction Pubs., 1997)
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