In 1995, the number of people dying from AIDS in the United States began to drop, and when deaths due to AIDS dropped in 1996, this was quickly offered as proof that the new drugs were working. As noted in this paper earlier, however, CDC statistics clearly show that new AIDS cases started dropping in 1993, several years before protease inhibitor cocktails were introduced which would seem the most obvious explanation. In addition, in 1993 the number of AIDS cases doubled overnight when the definition of AIDS was changed for the third time. Previous changes had resulted in more and more illnesses being officially dubbed "AIDS defining conditions", including things like certain yeast infections, cervical cancer and lymphoma which are relatively common in people of the same age group as most HIV positive people. Therefore, just about any serious condition that happens to occur in a person diagnosed "HIV positive" could now be officially blamed on HIV, along with any infectious process. The 1993 definition change included people who had low T-cell counts. The trouble is that a lot of these people were clinically completely health, which means that an artificial inflation of AIDS cases occurred. 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. 
So what studies do exist that support the widespread claims that new AIDS medications have revolutionized the treatment of AIDS. These claims are not based on any controlled studies, but rather on clinical observations and media reports. The accepted way to ensure that these anecdotal stories not a result of the placebo effect or observer bias is to perform "placebo controlled", randomized, double blind studies. These studies are sadly lacking in the case of protease inhibitor cocktails, AZT, and other AIDS drugs.
There have been a large number of studies looking at the effectiveness and safety of PI cocktails, but only two have actually looked at clinical health. All of the other ones focused exclusively on "viral load", which earlier sections of this book have revealed to be a questionable marker of HIV activity. A random testing of the population revealed that a large majority of people who have "viral loads" are HIV negative on the antibody tests, which is why the "viral load" test is only given to people who have already tested positive on the antibody tests. 
One would expect that lots of studies would be available documenting clear clinical benefits, but that is simply not the case. The fact that only two of the hundreds of controlled studies actually look at clinical health raises serious questions about whether bias and placebo response is involved in the anecdotal media reports of drug-related cures. Many such reports do not even mention clinical health, but refer to the "virus rebounding in their blood streams" as proof that people are getting sick. If one looks more carefully it is often obvious that the people in question are healthier without the drugs, because the drugs are associated with debilitating side effects in a majority of people who take them. One also must rightfully ask how this entire multi-billion dollar industry of anti-AIDS medications was established on statistically insignificant evidence. 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.
The two studies that do claim health benefits, and not just "viral load", are of minimal value (Hammer et al 1997, Cameron et al. 1998). They did not find statistically significant reduced death rates. Both were stopped early, which biases the results in favor of the drugs, since the study will be stopped at a statistically advantageous time. The Hammer study suffered from very incomplete reporting, making it difficult to assess toxicity or results. In addition, the Hammer study broke their own study design in order to increase their 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.
The second study by Cameron et al (1998) was of better quality, but its results suggest greater toxicity 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 th double-blind could be easily penetrated by both patients and clinicians. Fully 21% of the people taking the three drug combination dropped out of the study before the 4.5 months were up, which again hopelessly biases the results. In spite of all these favourable biases, although there was some 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 use a "placebo" which is actually 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 never, ever done. 
The argument thus far is simply that the new protease inhibitor cocktails are completely unproven, open to bias, and may be due to placebo effects. many prominent scientists, however, take the argument quite a bit furthur. 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".
Are the effects of AZT and other "antiretrovirals" being blamed on HIV?

Many people are more comfortable with a physical cause of disease, and thus might reject the idea that emotional, psychological, social, and spiritual influences could cause such devastating illness. People like this may be unconvinced by the portions of this book that deal with such "soft" sciences, but may still be curious what causes the symptoms in people diagnosed with AIDS, given the problems with the HIV hypothesis that I outlined in the first part of this book. To these people, the following section may make more sense. In the same way that some people question whether cases of "voodoo hexing" could actually be caused by poisoning, some people may question whether AIDS could be caused by poisoning. I again do not claim to "prove" the arguments here, but rather to present the evidence so that the reader can decide. I include a number of direct quotes to make this somewhat easier.
AZT, ddI, ddC , protease inhibitors and other drugs termed "antiretrovirals" have been hailed as breakthroughs in AIDS treatment. As described above, what may surprise just about everyone, including people who have been diagnosed "HIV positive" and their physicians, is that there is not even a single controlled study showing a statistically significant reduction in mortality using these agents. The studies used to test their efficacy rely exclusively on measurements of "viral load". The only studies published that claim positive outcome were short-term and did not have statistically significant results (Cameron et al. 1998, Hammer et al 1997). Even if they do have results, however, the possibility of a placebo response is a likely possibility, given the fanfare that has surrounded them since their introduction. Finally, because of the harsh side effects, it is unlikely that any kind of double-blind can be maintained in such a study.
In the opening segment of this book I cited a study from 1950 in which syrup of ipecac, which normally causes nausea and vomiting, cured women who were already suffering from nausea and vomiting (Wolf 1950). 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. After reading the following evidence, one may well see how this 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.
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 that under which these drugs are sold.)

1) 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."

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 this 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 fashion. (2) 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 Study, 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)

2) 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 1994. 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. 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 11 of 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 five years ago when high doses of AZT were regularly given to everyone diagnosed "HIV positive" whether or not they showed any sign of illness.

3) An article in the New England Journal of Medicine (4) 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.

4) "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 Neurology (5), 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 author's 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 critique (2).

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 documented in the main section of this book. 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 infection (8). 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 fundtioning 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.

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.

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 reached (1). 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. (For more discussion of the Concorde see appendix (1)(9)(10)

The idea that mutated strains of HIV are capable of causing health problems has been completely disproven by the work of David Rasnick, who published his results in the Journal of Biological Chemistry. (11). Thus, the decline seen in most patients is NOT due to "mutated HIV". A much more simple answer is that the combined effects described above finally take over completely, and often irrevocably.

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

References:

1) Lancet; 1998: Volume 352; Supplement 5.

2) These studies of T-cell damage are part of a comprehensive
discussion of the extreme toxicity of these drugs.
Pharmacology and Therapeutics 1992; Volume 55: 201-277. 

3) Annals of Hematology 1994; Volume 69: 135-138. 

4) New England Journal of Medicine. 1990; 322(16) : 1098-1105.

5) Neurology. 1994;Volume 44: 1892 -1900. 

6) Science. November 21, 1997; 278: 1399-1400.

7) Ader R, Felten DL & Cohen N. Psychoneuroimmunology. Second
Edition. San Diego: Academic Press, 1991 

8) Kolliadin V., DESTRUCTION OF NORMAL RESIDENT
MICROFLORA AS THE MAIN CAUSE OF AIDS, Aug. 1996
http://www.virusmyth.com/aids/data/vkmicro.htm

9) New England Journal of Medicine 1992; 326: 437-443

10) Lancet 1994; 343: 871-881.

11) Journal of Biological Chemistry 1997; Volume 272 No. 10: 
6348-6353.

United States Pharmacopeial Convention (1996). USP DI: Drug Information for the Health Care Professional, 16th Edition. pages 3032-3034.
 

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