In addition, in 1993 the number of AIDS cases doubled overnight when the definition of AIDS was changed for the third time. This is almost entirely because the 1993 definition change allowed people who had low T-cell counts, but no illnesses, to be listed as AIDS cases. Since then two-thirds of AIDS cases have been people who are clinically completely healthy. This created an artificial inflation of AIDS cases. These new cases were at low-risk, and thus the average life-expectancy of people diagnosed with AIDS would be expected to increase, no matter what medications were used. The CDC itself states that the new figures for AIDS prevalence have been artificially inflated by the definition changes:

"AIDS case reports received after January 1, 1993, were influenced by the expanded AIDS surveillance case definition and chiefly represent reporting of persons who had CD4+ cell counts below 200/uL with or without illness. This change greatly altered the pattern of case reports and was most pronounced in the first quarter of 1993."²¹

AZT, 3TC, d4T , protease inhibitors and other drugs termed "antiretrovirals" have been hailed as breakthroughs in AIDS treatment. So what studies exist that support the widespread claims that new AIDS medications have revolutionized the treatment of AIDS? One would expect a lot of very clear and striking study results showing reduced illness and reduced death with statistically significant reductions. To most people's surprise, a careful search of the medical literature finds that these claims are not based on controlled studies, but rather on clinical observations and media reports. This is not to say that there are no studies of protease inhibitor cocktails. The problem is that they all ignore clinical health, and instead focus on viral load. Only two controlled studies have actually looked at clinical health. All of the others focused exclusively on viral load, which has been shown to be a questionable marker for the presence of HIV, let alone for clinical health reduction (see Problems with HIV Science).

The two studies that do claim health benefits, and not just viral load reduction were published in 1997 and 1998 (Hammer, 1997; Cameron, 1998)^13,14. They did not find statistically significant reduced death rates. Both were stopped early, which biases the results in favor of the drugs. The Hammer study suffered from very incomplete reporting, making it difficult to assess toxicity or results. In addition, the Hammer study13 researchers broke their own study design in order to increase their study's statistical significance. By combining two separate treatment groups, the statistical "P value" was artificially increased. In addition, the gross underreporting of "AIDS-defining" events make this study of little or no value, since it only reports on one or two of the thirty one "AIDS-defining illnesses".

The second study by Cameron et al¹⁴ was of better quality, but many more of the study participants experienced toxicity rather than benefit. People given the full drug regimen had extremely high toxicities compared to placebo recipients, including 50% with diarrhea, another 52% with nausea, 29% vomiting, 28% circumoral parasthesia (numbness and tingling around the mouth), and 25% weakness. With these extremely high toxicities, it is easy to see how the double-blind could be penetrated by both patients and clinicians. Fully 21% of the people taking the triple drug combination dropped out of the study before the 4.5 months were up, which biases the results. In spite of all these favourable biases, although there was a reduction in opportunistic infections, the authors found little or no reduction in mortality, as a graph on page 546 clearly indicates. They mask this failure by lumping death statistics in with opportunistic infection statistics, citing reductions in the probability of "AIDS progression or death", a practice which seems designed to confuse or mislead people who read the study rather than to educate them. The toxicities described here occurred over the short space of 4.5 months, and the risk of giving these drugs for years on end has never been assessed.

Both these studies claim to have used a placebo (i.e. inert substance to take the place of an active medicine), but actually used a completely unproven combination of AZT with another DNA chain terminator like ddI or ddC. This alone eliminates these studies from any meaningful scientific discourse, unless the "placebo" combination has been shown to be at least safe, something that can only be done by testing it against a true placebo. This was not done.

One must rightfully ask how this entire multi-billion dollar industry of anti-AIDS medications was established with studies that have statistically insignificant results. When billions of dollars and thousands of careers are at stake, the potential for bias is enormous, and one must be very careful about making conclusions from such incomplete reporting.

Are the effects of AZT and other "antiretrovirals" being blamed on HIV?

The argument thus far is simply that the new protease inhibitor cocktails have not been proven to benefit patients. Many prominent scientists, however, take the argument quite a bit further. They argue that the very drugs used so wantonly with people diagnosed "HIV positive", could very well be causing much of the illness and death that is blamed on "HIV".

Although the newer "antiretrovirals" like ddC, ddI, and d4T, have analogous mechanisms of action and similar toxicities to AZT, they have not been studied as extensively and therefore are not discussed in as much detail in the studies outlined below. The major exception to this is "HIV Dementia" as discussed near the end of the essay. (See glossary of brand names below under which these drugs are sold.)

Glaxo Wellcome puts the following warning in large, bold-faced, capital letters at the start of the section in the 1999 Physician's Desk Reference that describes AZT (referred to under the name Retrovir or Zidovudine):

RETROVIR (ZIDOVUDINE) MAY BE ASSOCIATED WITH SEVERE HEMATOLOGIC TOXICITY INCLUDING GRANULOCYTOPENIA AND SEVERE ANEMIA PARTICULARLY IN PATIENTS WITH ADVANCED HIV DISEASE (SEE WARNINGS). PROLONGED USE OF RETROVIR HAS ALSO BEEN ASSOCIATED WITH WITH SYMPTOMATIC MYOPATHY SIMILAR TO THAT PRODUCED BY HUMAN IMMUNODEFICIENCY VIRUS.

AZT's brand names are Retrovir and Zidovudine, and it continues to be one of the most commonly used drug in people diagnosed HIV-positive. Up until 1993 it was used by itself, in about triple the dose used today, but today it is used in combination with other drugs. Many other drugs that are often used in combination with AZT used AZT as a model and have similar toxicities.

An earlier version of the Physician's Desk Reference, published in 1992 made the connection even clearer:

It is often difficult to distinguish adverse events possibly associated with Zidovudine administration from underlying signs of HIV disease or intercurrent illness.

Warnings like these should bring about a great deal of concern, especially given the litany of contradictions and confusion surrounding the science of "HIV" as the cause.

Allow me to translate some of the above warnings. "Granulocytopenia", also called "neutropenia" means that the primary cells of the immune system, neutrophils, have been depleted, along with some other cells, eosinophils and basophils, which are less numerous but still important to immune function. This condition can be mild, moderate, or severe. The clinical course of severe neutropenia, as described in the basic pathology textbook, Pathologic Basis of Disease by Robbins (5th Ed.), which is used in most medical schools to study pathology, describes what happens to people with severe neutropenia.

CLINICAL COURSE: The symptoms and signs of neutropenias are those of bacterial infections. ... In severe agranulocytosis with virtual absence of neutrophils, these infections may become so overwhelming as to cause death within a few days." (Robbins, p.631).

This sounds disturbingly similar to a description of AIDS. Although CD4 T-cells are the first cells supposedly attacked by "HIV", "later stages of HIV infection" are often associated with loss of neutrophils. Robbins also states, in italics, that "the most severe forms of neutropenias are produced by drugs." AZT was claimed to specifically attack HIV replication by interfering with DNA replication. What is not mentioned in any textbook is that AZT has been found in five studies performed after its rushed FDA approval to be equally toxic to T-cells, the very cells whose absence is blamed on HIV, by inhibiting T-cell DNA replication in exactly the same fashion². AZT may cause an initial increase in T-cells, but in relatively short time the T-cells, neutrophils, and other immune system cells begin to decline. This artificially increased T-cell count was shown to have no bearing on survival in the best and most well-controlled study available on AZT, the Concorde Study⁹, which also found that people who were given AZT earlier died faster. This study will be reviewed below.

Another strongly worded warning appears in the 1996 edition of the USP DI: Drug Information for the Health Care Professional:

Because of the complexity of this disease state, it is often difficult to differentiate between the manifestations of HIV infection [sic] and the manifestations of zidovudine (AZT). In addition, very little placebo controlled data is available to assess this difference. (pages 3032-3034)¹⁵

An example of a study that documented the toxic effects that AZT has on people's immune systems was published in the Annals of Hematology in 1994¹⁷. AZT was given to 14 health care workers who were exposed to HIV-contaminated blood through needle sticks and similar accidents. As we saw in previous studies, the likelihood of any of them contracting HIV is extremely remote, about 1 in 333, which is even less than the probablity of finding someone who is HIV positive when randomly picking from the general population^12,18,19. Thus it is no surprise that none of them actually became "HIV positive" as a result of their needle stick. This is not the reason for including this study here, however. This type of study is important because the toxicity observed cannot be blamed on HIV, as is quite likely to happen in people diagnosed "HIV positive", so the toxicities are openly admitted to be caused by AZT and documented as such. Fully half of the 14 workers had to quit the drug because of severe toxic side effects, and the study was stopped early before more damage was done. Only 11of the 14 people could continue to take the drug for more than four weeks. Neutropenia developed in 36% (4 of 11) of the people who completed 4 weeks of AZT treatment. The three people who could not make it to four weeks dropped out due to "severe subjective symptoms". One worker had to be stopped prematurely because his neutropenia was so severe that he developed an upper respiratory tract infection. What is truly remarkable in this study is that these side effects developed in only 4 weeks, while patients with "HIV positive" status often take AZT and other similar drugs for years. The dosage of AZT included in current protease inhibitor "cocktails" is much lower, which may be one reason why people are "living longer with HIV" today than they were when high doses of AZT were regularly given to everyone diagnosed "HIV positive" whether or not they showed any sign of illness.

An article in the New England Journal of Medicine⁴ looked at the muscle wasting caused by AZT and compared it to muscle wasting, called "myopathy", that has been presumed to be caused by HIV. Their comments in the abstract are revealing: "We conclude that long-term therapy with Zidovudine can cause a toxic mitochondrial myopathy, which... is indistinguishable from the myopathy associated with primary HIV infection...". Robbin's text on pathology also contains sections on mitochondrial myopathy, stating that this kind of muscle wasting results in severe weakness. It also states that "this group may also be classified as mitochondrial encephalomyopathies." Encephalomyopathy, in lay language, means widespread damage to the brain and spinal cord.

"HIV Dementia": Although most retrospective studies have not found AZT to be associated with "HIV dementia", these studies were uncontrolled and thus open to all sorts of confounding variables and biases. One of the better controlled studies did find that "HIV dementia" was twice as likely to happen in people taking AZT. In this study, published in the journal Neurology⁵, the authors state:

among subjects with CD4+ cell counts < 200/mm3, the risk of developing HIV dementia among those reporting any antiretroviral use (AZT, ddI, ddC, or d4T) was 97% higher than among those not using this antiretroviral therapy

Because the authors include only people with low CD4 T-cell counts in their comparison, it is less likely that people took AZT because they were already sick. They go on to discuss sensory neuropathy, which is a degeneration of sensory nerves:

In addition, the findings of our analysis seem to confirm previous observation of a neurotoxic effect of antiretroviral agents. Numerous studies have linked the use of ddI, ddC, and d4T to the development of toxic sensory neuropathies, usually in a dose-response fashion.

These studies are but a sample of the evidence that suggest that AZT and other "antiretrovirals" used as monotherapy or as parts of protease inhibitor cocktail regimens are causing a variety of AIDS-like symptoms which are being blamed on HIV. Unfortunately, the beliefs about HIV are so strong that many of the authors of the studies come out supporting the use of the drugs. A notable exception is the article in Pharmacology and Therapeutics, which provides a thorough and devastating critique².

Note: As this goes to press, a review just published (Ann Intern Med. 2000;133:447-454) reveals new evidence that "HAART may actually promote the clinical expression and development of [opportunistic] infections, as well as AIDS-related malignant conditions and other noninfectious diseases" This review article cites 95 references, where authors list several opportunistic infections and malignancies usually known as AIDS defining conditions that afflicted patients only after initiation of HAART therapy lowered viral load and increased CD4 cell counts. See Appendix 3.

A LIKELY EXPLANATION FOR THE "COURSE" OF AIDS

Based partly on this evidence, a compelling argument can be made that much of what we call AIDS is a self-fulfilling prophecy which might happen as follows:

a) The severe, acute psychological stress of being diagnosed "HIV Positive" is quickly transformed into a severe, chronic psychological stress of living with a prediction of a horrifying decline that could start at any time. This causes a suppression of the immune system, with selective depletion of CD4 T-cells, as is well documented in the field of Psychoneuroimmunology⁷. In addition, people are more likely to be tested for HIV when there is already some health problem present, so that the psychological stress adds to significant stress due to the illness already present. These illnesses are often severe and chronic in nature. It is not necessary, however, for prior illness to be present. These factors have been studied in healthy people where they create the very same immunosuppression and immune dysregulation that may later be called "AIDS".

b) After testing positive, people are often put on a variety of powerful medications as a preventative measure and/or for treatment of actual infections. These include long-term regimens of the most potent broad-spectrum antibiotics, as well as "antiretroviral" agents like AZT, ddI, ddC, and protease inhibitors. Although the toxicities of the "antiretrovirals" have been outlined above, antibiotics also often have debilitating side effects which are easily blamed on HIV, including immune suppression. Perhaps more significantly, they lead to a complete disruption of the normal microbial flora present in the gastrointestinal system. The healthy balance of flora in the gastrointestinal tract and elsewhere in the body is one of the most important protectors against infection⁸. If this is not enough, these antibiotics also often lead to the development of multidrug-resistant strains of bacteria, fungi, and viruses, which can later ravage a person's system, especially if their immune system is not functioning very well.

c) Once the immune system starts to crack under the strain of the emotional stress, previous health problems (if there were any), and disrupted natural defenses, the diagnosis of AIDS is made. If not already on "antiretrovirals", then the person will now definitely be started on them, with all of the toxic effects described above.

d) The new "cocktails" are to be given until the patient dies, with no exceptions*, if possible. This is because of the theory that mutant, drug resistant, HIV will flourish if they go off of their treatment. Patients who abandon "antiretroviral" treatment would then, theoretically, be a public health threat because they might infect others with their superpowerful, mutated "HIV". Thus, aside from considering their own health, the patient has a larger social responsibility to stay on the "cocktail", no matter how debilitating the "side effects" are. It is heavily stressed that the patient must not miss a single dose, if at all possible. When the patient's health begins to fail, the failure is blamed on the effects of this "mutated HIV", possibly due to the patients poor compliance. Rarely are the drug toxicities and complications caused by the treatment held responsible.

* Recently, HIV specialists have begun to relax the demand for rigid adherence to treatment. They have started prescribing "strategic treatment interruptions" to allow patients to recover from drug toxicity and to see if their "restored" immune systems can cope unaided. [editor's note] See Appendix 3.

The idea that mutated strains of HIV are capable of causing health problems has been disproven by the work of David Rasnick, a scientists who holds nine patents in protease inhibitor research. Dr. Rasnick, who published his results in the Journal of Biological Chemistry¹¹, strongly disagrees with claims that protease inhibitors are helping people diagnosed "HIV positive", and instead maintains that they are causing symptoms blamed on HIV. His research shows that any decline in health is not due to "mutated HIV", and that the protease inhibitor cocktails themselves are more likely culprits.

Some people seem to respond well (at least temporarily) to these "antiretroviral" regimens. The reasons for this are unclear, but may be related to:

1. Direct actions of the drugs on many possible pathogens (including, possibly, HIV).
2. Toxic substances have been observed to stimulate the release of T cells from the bone marrow, before eventually exhausting the supply and causing immune cell depletion and anemia. The initial rise in CD4 counts seen in this case would be interpreted as improved immune function when it is actually the beginning of immune exhaustion.
3. Relief of the severe psychological stress due to the powerful belief that these drugs are "life-saving". This is often reinforced by rising CD4 counts and falling "viral load", which are doubtful and non-specific markers of actual health.
4. In a study from 1950 syrup of ipecac, which normally causes nausea and vomiting, cured women who were already suffering from nausea and vomiting¹⁶. The women were told that it was a new drug that eliminated nausea and vomiting, and this belief was apparently powerful enough so that their symptoms went away. Thus it was shown that if people believe in a drug, it can have positive effects, at least for a short while, even if it is normally highly toxic. If administered over a longer period, however, the initial benefit may fade, while the toxicities remain. This phenomenon could explain the anecdotal stories of success with AZT and other "antiretrovirals", as well as how some of the toxic symptoms caused by these drugs, could be later blamed on HIV.

Scientific studies attempting to document positive effects of protease inhibitor (PI) "cocktails" are of questionable value. Every one has been stopped early, like stopping a sporting event when the home team is ahead. This skews any attempt at finding benefit. Even worse, all of the studies of protease inhibitor combination therapy have been stopped before statistically significant reductions in mortality is even reached¹. In addition, the control groups' "placebos" were 2 antiretroviral drugs with no protease inhibitor. If the "antiretrovirals" are part of the problem then these so-called "placebo controlled" trials will not reveal it very well. Stopping the trials early was also the case with AZT monotherapy, until the Concorde study finally went to completion and found greater deaths and "adverse events" in the group that got AZT as a preventative measure. The other group, in which people were only given AZT after being diagnosed with an AIDS-defining condition, had about 25% fewer deaths. Of the 172 Concorde participants who died all but 3 were on AZT at some point^1,9,10. (For more discussion of the Concorde see Appendix 1)

Appendix 1: Concorde: MCR/ANRS randomized double-blind controlled trial of immediate and deferred zidovudine [AZT] in symptom-free HIV infection. Although the difference in survival between the participants who started AZT immediately (Imm) and those who were deferred (Def) until the onset of AIDS-Related Complex (ARC) or AIDS was not considered significant by the Concorde report (estimated 3-year probabilities of death were 8% Imm and 6% Def), other "events" were. "Adverse events", such as leukemia, anemia, neutropenia, etc., were at least 300% higher in the Imm group over the three year trial. A fact that is often missed when reading the Concorde report is that of the 172 (96 Imm, 76 Def) participants who died all but 3 were on AZT at some point. This is because 418 participants in the Def group switched to AZT part way through the trial; 74 for "personal reasons", 204 due to low CD4 count and only 109 (26%) due to progression to ARC or AIDS, which was the point of the trial. Ironically, one of Concorde's finding was that CD4 counts are not a useful marker for disease progression. In other words, people who weren't really sick were put on AZT, their T-cells rose, and in spite of this more of them had "adverse events" and more of them died. Was the cause of death HIV or AZT? (9)

Appendix 2: Glossary of generic & brand names, (class of drug) for "antiretrovirals"

3TC: Epivir®, lamivudine (NA)
abacavir: Ziagen® (NA)
AZT: ZDV, Retrovir®, Zidovudine (NA)
ddI: Videx®, didanosine (NA)
d4T: Zerit®, stavudine (NA)
delavirdine mesylate: Rescriptor® (NNRTI)
efavirenz: Sustiva® (NNRTI)
indinavir sulfate: Crixivan® (PI)
nevirapine: Viramune® (NNRTI)
nelfinavir mesylate: Viracept® (PI)
ritonavir: Norvir® (PI)
saquinavir mesylate: Invirase®, Fortavase® (PI)
Combivir®: combines AZT & 3TC (NAs)

Appendix 3: Inflammatory Reactions in HIV-1-Infected Persons after Initiation of Highly Active Antiretroviral Therapy
Joseph A. DeSimone, MD; Roger J. Pomerantz, MD; and Timothy J. Babinchak, MD
Ann Intern Med. 2000;133:447-454.
This is a review article with 95 references, where authors list several opportunistic infections and malignancies usually known as AIDS defining conditions that afflicted patients only after initiation of HAART therapy lowered viral load and increased CD4 cell counts. HIV researchers have created an ironic new name for this: "Immune Restoration Syndrome". The authors of this review state: "Although patients receiving HAART have reduced plasma HIV-1 viral load and increased CD4+ T-lymphocyte counts, they still develop AIDS-defining events, particularly in the first 2 months of treatment. A delay in restoration of immune function may account for the development of opportunistic infections. It is possible, however, that HAART may actually promote the clinical expression and development of such infections, as well as AIDS-related malignant conditions and other noninfectious diseases. Several authors have recently reported cases that may represent progression of previously quiescent disorders to symptomatic diseases after initiation of HAART."

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