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To Nicholas Bennett et al,
I have always approached this issue with an open mind. In many respects I have truly wanted to be completely convinced that HIV does cause AIDS because that is what my training had always taught me. But is also taught me that consensus science CAN be wrong science and that experts CAN be wrong. Usually that happens when a prevailing scientific discipline was the “science du jour” and scientists became locked into one -dimensional thinking. That is never a good thing.
At what point should one stop questioning? It is a difficult question to answer. Does science need to prove something absolutely before it is accepted as a truth? I think not – that is rarely done. When science influences medicine, when does one decide that the weight of evidence is adequate to make treatment decisions? Clearly the first trial of AZT did not prove its risks outweighed its benefits. The trial was compromised because the blind was broken. Several of those who took AZT had to receive blood transfusions to stay alive because of the toxic effects of the drug. Nevertheless, it was still approved. Was that good science?
A physician named Dr Roberto Giraldo, is alleged to have tested many blood specimens (including his own) via the standard ELISA protocol. Some were positive and others were not positive. He then tested the same specimens without diluting the blood and they were all positive, including his own. Was that good science? It certainly seemed to suggest that the ELISA for HIV was not specific and more like an ESR test than a test for a specific antibody. Was that good science?
In response to my comments re the rates of HIV in children and the elderly, Nicholas Bennett wrote:
“As an example, if there were a 5-6% false positive rate, the childhood and elderly rates would practically disappear from the Mandela study whereas the young adult rates would be (say) around 20% instead of 26%. Does this undermine the entire premise, or just the population estimates? “.
I guess that depends upon how one interprets a result like that. Does it mean that we can just subtract 6% form 26% and say that the remaining 20% are real positives OR does it mean that because 100% of the positives in children are false positives, then 100% in the young adult are also false positive. Or, perhaps if it is a measure of the inflammatory state of the immune system, then young children, who have had less exposure to the agents that cause the pro-inflammatory state, have a lower number. As one becomes exposed for longer periods (young adults) the pro-inflammatory state is heightened and you have a higher number. As you age, and the immune system becomes less capable of responding, the number starts to fall off again. That seems to make sense too. So are HIV tests measuring HIV or?
In a very recent article in the Journal AIDS (For more information, see AIDS, Volume 18 (1) 2 January 2004) the authors question the benefits of a life-long treatment for HIV infection. The article indicates that HAART has no effect on viral load after three years of use and confirms that T cell count gains taper off after just 18 months on the meds. They note that "given the side effects...such as lipodistrophy, metabolic disturbances, increased cardiovascular risk, mitochondrial toxicity and altered quality of life ….. it is more and more difficult to imagine anti- HIV treatments as life-long prescriptions. The inconvenience of long-term treatment may outweigh the benefit of maintaining the CD4 cell count at a high level considering that treatment beyond 2 to 4 years will NOT result in a significant reduction of viral load.” What impact if any will this science have on HIV treatment? (I want to indicate that I have not read this paper – this information was passed to me very recently by a friend).
If the above is correct, then how does the medical community account for the long-term survivability they assign to HAART therapy? This seems to suggest that after 18 months, CD4 counts are already falling again and there is little impact on viral load after 36 months. Yet we hear that because of these drugs, ill people are now surviving for many years. It seems that this long-term survival is independent of the impact of HAART on CD4 counts and viral load. If that is the case, then either HAART Tx is effecting some sort of as yet undiscovered benefit, or perhaps something else is altering the survival rates.
Why does one have AIDS in the US if their T-cell count falls below 200, but not in Canada. Are Canadians more hardy – I hardly think so. How can the same disease be diagnosed with such diversity.
In any event, I'd be interested to hear anyone's feedback on some of these issues.
Competing interests: None declared