HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS

Posts Tagged ‘HAART’

Poison in South Africa

Posted by Henry Bauer on 2008/10/26

Several publications have attempted to calculate the precise life-saving benefits of antiretroviral drugs (Walensky et al., Journal of Infectious Diseases 194 [2006] 11-19; Antiretroviral Therapy Collaboration, Lancet 372 [2008] 293-99; Bhaskaran et al., JAMA 300 [2008] 51-59). All of them are based on rather elaborate computerized models replete with hordes of assumptions, and they deliver outputs that not only differ with one another [numbers are cited in “HAART saves lives — but doesn’t prolong them!?”, 17 September 2008] but that are also at stark variance with plain facts adduced quite directly from observations on patients:
1. The Antiretroviral Therapy Cohort Collaboration (Lancet 2006; 368: 451–58) analyzed data from more than 22,000 patients on HAART and found that the therapy decreased viral load “but such improvement has not translated into a decrease in mortality”; in other words, no life-saving benefit at all.
2. Death statistics for the USA show that, even by 2004, half of all HIV/AIDS patients were dying at or below age 45. Since the introduction of HAART in 1996, both the average time between a diagnosis of AIDS and death and the very slow and steady changes in median age of death from 1982 to 2004, refute the claim that HAART renders “HIV/AIDS” a chronic but manageable disease that offers prospects of virtually a normal life-span [“HAART saves lives — but doesn’t prolong them!?”, 17 September 2008].

Since the observed facts contradict the estimates, the only thing demonstrated by those calculations of supposed benefits from HAART is that one can obtain any desired result from a computer model if one uses a sufficient number of suitable assumptions; and the only thing that consumers of such outputs need to remember is GIGO: Garbage In, Garbage Out [“Antiretroviral therapy has saved 3 million life-years”, 1 July 2008].

To the spurious claims of life-saving benefits from HAART, there has now been added (biology news net) an even more dubious extrapolation: Those supposed benefits have been (mis)applied to calculate how many South African lives could supposedly have been saved, if antiretroviral drugs had been distributed sooner and more widely (Chigwedere et al., JAIDS, online publication ahead of print, 10.1097/QAI.0b013e31818a6cd5) . The overall assumptions are indicated (indicted?) already in the Abstract [emphases added]:

Using modeling, we compared the number of persons who received ARVs for treatment and prevention of mother-to-child HIV transmission between 2000 and 2005 with an alternative of what was reasonably feasible in the country during that period”.

“In 1999, President Thabo Mbeki, under pressure to provide zidovudine (ZDV or AZT) for prevention of mother-to-child HIV transmission (PMTCT) and AIDS treatment, announced that the drug was toxic and dangerous to health and that the government was not going to provide it”; thus implying that AZT is not toxic — or, at least, as though this somehow doesn’t matter: “its side effects were clearly documented and disclosed”, citing for the latter a 1987 paper (Richman DD, Fischl MA, Grieco MH, et al. The toxicity of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex: a double-blind, placebo-controlled trial. N Engl J Med. 1987;317:192–197), one of whose authors (Fischl) had subjected Kim Bergalis to such high doses that she died within a couple of years (“The Stories of Those Who Believed in AZT”, Peter Duesberg; several cases are described in “The cure that failed”, Tom Bethell, National Review 10 May 1993).

In case the latter reports of AZT toxicity appear to come from biased sources, have a long look at the official Treatment Guidelines.  One of the “Factors associated with immunologic failure” — i.e., likely causes of destruction of the immune system — is “Medications, both antiretrovirals (ZDV [270], TDF + ddI [271-273]) and other medications” (p. 37). AZT/ZDV is also responsible (Tables 9 & 10) for “Rare but serious cases [i.e., potentially fatal] lactic acidosis with hepatic steatosis”, bone marrow suppression, anemia, mitochondrial toxicity (which can cause hepatic steatosis); in combination with other “life-saving” antiretroviral drugs, “Hypersensitivity reaction that can be fatal” (Table 10). Among the “Potentially Life-Threatening and Serious Adverse Events” (Table 18a), ZDV features under “Lactic acidosis, hepatic steatosis, pancreatitis (severe mitochondrial toxicities)”, “Stevens-Johnson syndrome (SJS), Toxic epidermal necrosis (TEN)”, bone marrow suppression, “Hepatotoxicity (clinical hepatitis or asymptomatic serum transaminase elevation)”. Among the less serious “side” effects “Compromising Quality of Life and/or With Potential Impact on Medication Adherence” (Table 18c), ZDV features as causing “fat maldistribution”.

In other words, contrary to what is implied by Chigwedere et al., ZDV is toxic to a potentially fatal degree. That’s also admitted implicitly by some number of mainstream researchers, even some who claim benefits from HAART, for example, Walensky et al. (Journal of Infectious Diseases 194 [2006] 11-19) whose calculation of supposed benefits of antiretroviral drugs ascribes no benefit at all to AZT/ ZDV treatment from its introduction in 1987 up to the era of HAART. The immediate drop in death rate when ZDV monotherapy was stopped is yet another direct measure of the drug’s toxicity [“HAART saves lives — but doesn’t prolong them!?”, 17 September 2008].

It would be wearisome as well as pointless to cite the innumerable presumptions and assumptions in Chigwedere et al., but I can’t resist pointing to the throw-away phrase highlighted in the following passage:

“we estimated the average life-years that ARV therapy adds to patients with AIDS in Africa. Primary studies done in Africa (including South Africa), a meta-analysis, and a comparison with the developed countries show that other than increased mortality at the start of treatment, patient responses to ARV treatment in Africa are similar to those observed in the developed world. 20”

Reference 20 is Braitstein P, Brinkhof MW, Dabis F, et al; Antiretroviral Therapy in Lower Income Countries (ART-LINC) Collaboration; ART Cohort Collaboration (ART-CC), “Mortality of HIV-1-infected patients in the first year of antiretroviral therapy: comparison between low-income and high-income countries”, Lancet 367 [2006] 817-24; the pertinent information is “Mortality was higher in low-income settings (124 deaths during 2236 person-years of follow-up) than in high-income settings (414 deaths during 20 532 person-years)”. In other words, in Africa 14.9 of every 100 people treated with HAART die in the first year of treatment, whereas in the developed world only 2 of every 100 people treated with HAART die in the first year of treatment.

Now, that throw-away reference by Chigwedere et al. implies that response to HAART after the initial deaths has been found to be similar in low-income settings to that in high-income ones, but the cited reference doesn’t exactly say that. The ratio of deaths at 9 months is indeed lower than initially, but it is still between 1.5 and 2 times (adjusted and unadjusted hazard ratios respectively) higher in the low-income countries; whether 1.5-2 is  “similar” to 1 is a matter of opinion. Nor is there any obvious reason to assume that the decrease to month 9 will continue thereafter; for example, I might speculate that since the Africans beginning treatment are initially ill, whereas about 70% of those entering treatment in the United States are not ill (asymptomatic HIV-positive with CD4 <200), the Africans would be more likely to succumb to the “side” effects of the drugs, so that the mortality ratio would increase again after its initial decline during the brief exposure of 9 months — almost at once, the most seriously ill Africans succumb to the poisonous drugs, and those who are not so ill succumb more slowly but still appreciably more quickly than in the United States.

In any case, the vastly different criteria for beginning treatment in low- and in high-income countries, and the vast difference in disease burdens of many kinds — both acknowledged in the cited article — suggests that the attempt to extrapolate to low-income settings the benefits calculated for high-income settings is in itself invalid a priori — doubly so, of course, since the benefits calculated for high-income settings are spurious, as shown (see above) by the direct data on >22,000 patients from the Antiretroviral Collaboration and the death statistics for all HIV/AIDS patients in the United States: half the deaths from “HIV disease”, even by 2004, occurred by age 45.

Nor are the technical deficiencies in Chigwedere et al. the only reason to discredit their conclusions. One might also note that the authors lack any credentials to discuss such matters of economic and political policy as “what was reasonably feasible in the country during that period”, which is the whole point of the article. Indeed, one might question the very purpose of publishing these calculations. Even were they impeccably correct technically, they add nothing — and claim to add nothing — of medical or scientific relevance. This is an exercise in propaganda and politics, hardly appropriate for a journal whose raison d’être is described thus:  “JAIDS Journal of Acquired Immune Deficiency Syndromes , non-HIV, and AIDS-related information from all relevant clinical and basic sciences, with a strong focus on molecular biology, cell biology, epidemiology, and clinical virology. Each issue of JAIDS publishes vital information on the advances in diagnosis and treatment of HIV and non-HIV infectious [sic], as well as the latest research in the development of therapeutics and vaccine approaches”. (The reference to “non-HIV” is curious: do they want the Journal to be able to continue even after HIV has been shown not to cause AIDS?) The 3 editors-in-chief specialize in “Basic Science Articles: David D. Ho, M.D. . . . Clinical Articles: Paul A. Volberding, M.D. . . . Epidemiology Articles: William A. Blattner, M.D.”, which brings to mind not only the incongruity of an article on public policy but also what I’ve said about doctors as scientists [“Nobel Prizes Illustrate that Doctors are Not Scientists”, 19 October 2008].

But I’d like to reiterate the main point, which cannot be overemphasized. A decade after the introduction of HAART, we know that its theoretical basis is wrong [“HAART and HIV/AIDS: Dilemmas, Paradoxes, and Errors”, 12 October 2008], and we know that half the people whose lives are being supposedly saved by HAART meet their death by age 45 [“HAART saves lives — but doesn’t prolong them!?”, 17 September 2008]. No amount of sophisticated computer modeling can gainsay those facts.

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HAART and HIV/AIDS: Dilemmas, Paradoxes, and Errors

Posted by Henry Bauer on 2008/10/12

“The Sink and the Murder Scene: Rise and Fall of a Causal Model for AIDS Pathogenesis” by Vincenzo Crupi (Logic and Philosophy of Science V [#1, 2007] 9-32)  is a clear, concise, fully documented summary of what’s missing in our understanding of several aspects of “HIV” and of “AIDS”; and it illustrates, in my opinion, what’s very wrong with “HIV = AIDS” and “highly active antiretroviral treatment”.

From the very beginning, the central problem has been to understand how “HIV” kills the immune system. That it does so was assumed because of a correlation between CD4+ counts and disease progression (a correlation that has turned out to be anything but consistent) and an apparent preferential association of HIV with CD4+ cells. But — as Duesberg, for one, pointed out early on — a negligible proportion of CD4+ cells in AIDS patients is actually “HIV-infected”. Even in lymph tissue, which was suggested to be a “reservoir”, only about 1% of cells are “HIV-infected”.

To resolve this decade-long dilemma, Ho and Shaw invented a model in which the very low steady-state or average “infection” rate masked an enormously high rate of cell death and replenishment whereupon, after the average “latent” period of about 10 years, the immune-system was exhausted and could no longer replenish. Crupi shows, with citation as well as explication of sources, that this model is disproved by published observations and experiments. Among the salient points is that CD4+ counts in the blood can be misleading because these cells are redistributed as needed throughout various parts of the body (as mentioned previously on this blog in relation to Juliane Sacher’s work — “AIDS as Intestinal Dysbiosis”, 23 February 2008; “Alternative Treatments for AIDS”, 25 February 2008. Moreover, antiretroviral drugs may quickly reduce “viral load” without increasing the life-span of the cells supposedly killed by the virus, indicating that “HIV” is not the agent of cell death.

Because of these findings, mainstream speculation turns increasingly to the view that AIDS is characterized by “abnormal, chronic and up-regulated levels of immune system activation”, which may also occur in absence of HIV. Furthermore, clinical improvement can occur in AIDS patients on antiretroviral therapy even when “HIV” seems little affected. Crupi concludes that research is urgently needed on some of the matters that mainstream HIV/AIDS researchers have largely by-passed.

I strongly recommend this article. The facts about “HIV/AIDS” are at least equally well explained by regarding “HIV” as a sign of immune activation — or physiological stress, or specifically oxidative stress as the Perth Group has it — as by the apparently current mainstream view that “HIV” causes the immune activation that indirectly and eventually depletes the immune system.

I think it’s worth noting that HAART, “highly active antiretroviral treatment”, was designed on the basis of the Ho-Shaw model, which has been thoroughly disproved. It does not necessarily follow that HAART is ineffective, of course — it might by chance have some benefits, it would not be the first medical treatment to work despite misunderstanding or lack of understanding of why it works. As it turns out, though, death statistics  show that HAART doesn’t prolong lives to any significant extent. The discussion and citations in Crupi’s article serve to explain why that’s the case.

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Antiretroviral treatment benefits? from 3 MILLION to 1.2 million to …!?!

Posted by Henry Bauer on 2008/07/18

The claim by Walensky et al., triumphantly cited by Anthony Fauci, was that “at least 3 million” life-years had been saved by antiretroviral drugs since 1989. The fine print, however, noted that only 1.2 million of those had already been realized, the remainder were expected to be accruing to currently living HIV/AIDS patients [HIV/AIDS SCAM: Have antiretroviral drugs saved 3 million life-years?, 6 July 2008]. Now I come across information showing that even this 1.2 million overstates matters.

The total benefit claimed by Walensky was calculated by them for 6 eras of treatment approach:
Let’s assume PCP prophylaxis yielded savings of only 3.1 months per person in later eras as well as in the first. Then the savings attributed to it amount to 58,000 years in the 2nd era, 19,000 in the 3rd, 14,000 in the 4th, 19,000 in the 5th, and 6,000 in the 6th, giving a total (including the 41,000 in the first era) of 157,000 life-years saved through PCP prophylaxis alone.

But how did Walensky et al. decide that PCP prophylaxis had this survival benefit? Their leading reference regarding PCP prophylaxis is:
“2. Ioannidis JP, Cappelleri JC, Skolnik PR, Lau J, Sacks HS. A metaanalysis of the relative efficacy and toxicity of Pneumocystis carinii prophylactic regimens. Archives of Internal Medicine; 156 (1996) 177–88.”

That article analyzed 35 randomized trials. It excluded one of those from mortality considerations because “mortality data were dominated by the early trial of Fischl et al. (15) in which the mortality from PCP was 50% and PCP accounted for 29% of all deaths in the placebo group. When this study was excluded, prophylaxis . . . offered no survival benefit over placebo (risk ratio 1.00 [95% CI, 0.72 to 1.39]). Similarly, no significant difference was seen in overall mortality among different prophylactic regimens”.
The Fischl trial was of a cohort of people already diagnosed with Kaposi’s sarcoma; Fischl et al., JAMA 259 [1988] 1185-9. Half of those treated with Bactrim prophylaxis had “adverse reactions”. The authors commented that this drug is known to cause bone-marrow suppression, which would be enhanced by the antiretroviral then in use, AZT = zidovudine, which has the same “side”-effect.

In concluding comments, Ioannidis et al. again note the lack of survival benefit: “P carinii prophylaxis significantly reduced P carinii events and P carinii-related deaths, but there was no statistically significant reduction in the overall mortality of patients who received prophylaxis”.

Evidently the estimate of benefits of anti-HIV treatment needs to be further reduced below 3 million 1.2 million.

In every form of treatment, what matters to patients is quality of life and a possible reduction in all-cause mortality: it’s no gain if one dies just as soon or sooner from the drugs than from the ailment. It is by no means routine, unfortunately, for all-cause mortality to be reported in clinical trials; that lack is emphasized in Joel Kauffman’s rigorously researched book, Malignant Medical Myths.

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