Can AZT and Other “Antiretrovirals” Cause AIDS?

January 1, 2008

2 Jan (MERCOLA) – The truth is that AZT, ddI, ddC , protease inhibitors and other drugs termed “antiretrovirals” have not been found in any controlled studies to show proven clinical benefits for HIV/AIDS patients. The only studies published that claim positive outcome were short-term and did not have statistically significant results.(1)

Even more alarming, there is plenty of evidence that these drugs have been found to cause the very symptoms they are meant to cure.  Over 500 M.D.s’ and/or Ph.D.’s have signed a statement calling for a reappraisal of the causes of AIDS, and questioning whether the symptoms are being caused by 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.

1. Glaxo Wellcome puts the following warning in large, bold-faced, capital letters at the start of the section in the 1998 Physician’s Desk Reference that describes AZT (brand name Retrovir or Zidovudine).


Please allow me to translate. “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.

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. Robbins also states, in italics, that “the most severe forms of neutropenias are produced by drugs.” 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.(2) This is not surprising since T-cells are produced in the bone marrow, and all the other cells produced there are depleted by AZT. AZT may cause an initial increase in T-cells as the body’s immune system responds to the toxic stress being placed on it by AZT, but in relatively short time the T-cells, neutrophils, and other immune system cells begin to decline.

2. An example of a study that documented the effects of AZT on people’s immune systems was published in the Annals of Hematology. (3)

AZT was given to 14 health care workers who were exposed to HIV contaminated blood through needle sticks and similar accidents. This type of study is important because the toxicity observed cannot be blamed on HIV, as is quite likely to happen in HIV positive people. 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. Neutropenia (as described above) developed in 36% (4 of 11) of the people who completed at least 4 weeks of AZT treatment.

3 of the 14 people could not even make it to four weeks 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 these fare better when compared with treatment that uses AZT by itself.

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”, 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”

They also discuss sensory neuropathy, or degeneration of sensory nerves stating:

“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 study in Pharmacology and Therapeutics, which provides a thorough and devastating critique (2).

Another fact that raises serious questions about the possibility of HIV causing disease is the fact that even after some $45 billion dollars of research funds, scientists cannot figure out how it supposedly destroys T-cells. This is because it does not destroy T-cells in test tubes and has never been shown to destroy them in humans, either.

At a conference in 1997, as reported in the journal, Science, this fact was made very clear as the theories espoused by David Ho et al. were revelaed to have serious flaws. As stated in the Science article “Yet the central; mystery of AIDS remains unresolved: How does the virus cause the severe loss of T-cells… which is the hallmark of the disease?”

An immunologist from Harvard Medical School, as quoted in the same article, summed up the problem as follows: “We are still very confused about the mechanisms that lead to T-cell depletion, but at least now we are confused at a higher level of understanding” (6). A simpler explanation of these problems, especially after $45 billion, is that HIV does not affect T-cells, at all.


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 dangerous suppression of the immune system.

This immunosuppressive effect of chronic psychological stress is well documented in scientific studies and also is a common part of most people’s personal experience (7). 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) Once tested, people are often put on long-term and high doses of the most potent broad-spectrum antibiotics, if not antiretrovirals also, as a preventative measure and/or treatment for illnesses.

These antibiotics often have debilitating side effects which are easily blamed on HIV, including immune suppression. Perhaps more significantly, they lead to a complete disruption of our normal microbial flora. The healthy balance of flora in our gastrointestinal tract and elsewhere is one of our most important protectors against infection (8).

On top of all this, these antibiotics also often lead to the development of multidrug-resistant strains of bacteria, fungi, and viruses. 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.

Then the person is started on the “antiretrovirals”, if not already on them, whose toxic effects are described above. More and more people are being placed on these drugs when they are still healthy and have not been diagnosed with “AIDS”. 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 “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”, it is heavily stressed that the patient must not miss a single dose. 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 is interpreted as improved immune function.
  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 when the “home team” is ahead. This skews any attempt at finding benefit in the same way that continually stopping sporting events as soon as the home team is ahead would. Even worse, all of the studies of protease inhibitor combination therapy have been stopped before statistical significance 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. 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.


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


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