HIV/AIDS Skepticism

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

Posts Tagged ‘Paul E. Sax’

HAART saves lives — but doesn’t prolong them!?

Posted by Henry Bauer on 2008/09/17

Death rates are down, yet AIDS patients are not living longer! Why not?

(This is a long post, and includes at least one Table that is too large to be viewed conveniently in the same window as the text. If you prefer to read it as a pdf, here it is: haartdoesnt-prolong-lives)

In the early 1980s, a diagnosis of “AIDS” typically had been followed by death within a year or two. At that time, diagnosis was on the basis of Kaposi’s sarcoma or of manifest opportunistic fungal infections — Pneumocystis carinii pneumonia or candidiasis.

Following the adoption of “HIV-positive” as a necessary criterion for an AIDS diagnosis, an increasing range of non-opportunistic infections and other illnesses came to be included as “AIDS-defining” (for instance, tuberculosis, wasting, cervical cancer, etc.) — see Table 1; the most consequential changes were in 1987 and in 1993. The only basis for them was that people with some illnesses were quite often “HIV-positive”, in other words, there were correlations with “HIV-positive” status, not any proof that “HIV encephalopathy”, “HIV wasting disease”, or other additions to the list of “AIDS-defining” conditions were caused by “HIV”. Indeed, there could not be such proof since mechanisms by which “HIV” could cause illness have not been demonstrated, and they remain to this day a matter for speculation — even over the central issue of how HIV (supposedly) kills immune-system cells. An absurd consequence of these re-definitions, often cited by HIV/AIDS skeptics, is that a person suffering indisputably from tuberculosis (say) might or might not be classed as an HIV/AIDS patient, depending solely on “HIV” tests.

Table 1

(from Nakashima & Fleming, JAIDS 32 [2003] 68-85; numbers in parentheses after the dates refer to sources cited in that article)

As “AIDS” was being diagnosed increasingly among people less desperately ill than the original AIDS victims, survival time after diagnosis became longer.

The 1993 change extended the umbrella of “AIDS patient” to cover people with no manifest symptoms of ill health; in ordinary parlance, they weren’t ill, and consequently the interval between an AIDS diagnosis and death was bound to increase dramatically. This re-definition also expanded enormously the number of “AIDS cases”: about 70% of them are not ill (Walensky et al., Journal of Infectious Diseases 194 [2006] 11-19, at p. 16).

In 1996, earlier treatment for AIDS with high-dose reverse transcriptase inhibitors like AZT (ZDV, Retrovir) was increasingly superseded by “highly active antiretroviral treatment” (HAART), which has been generally credited with the prolonging of lives by a considerable number of years. According to the Antiretroviral Therapy Collaboration (Lancet 372 [2008] 293-99), life expectancy for 20-year-old HIV-positives had increased by 13 years between 1996 and 2005 to an additional 49 years; for 35-year-olds, the life expectancy in 1996-99 was said to be another 25 years. According to Walensky et al. (op. cit.), survival after an AIDS diagnosis now averages more than 14 years. Yet another encomium to antiretroviral drugs claims that “by 2004-2006, the risk of death in the first 5 years following seroconversion was similar to that of the general population” (Bhaskaran et al., JAMA 300 [2008] 51-59).

There is general agreement, then, that antiretroviral treatment has yielded substantial extension of life to people already diagnosed with AIDS. The interval between an AIDS diagnosis and death should now be measured in decades rather than a year or two.

As with so many other contentions of orthodox HIV/AIDS belief, however, this expectation is contrary to actual fact. The greatest risk of death from “HIV disease” comes at ages in the range of 35-45, just as at the beginning of the AIDS era. There was no dramatic increase in median age of death after 1996 following the adoption of HAART, see Table 2:

Table 2
Age Distributions of AIDS Diagnoses and AIDS Deaths, 1982-2004
from annual “Health, United States” reports

The slow, steady increase in median ages of AIDS diagnosis and of death shown in Table 2 is pictured in Figure 1, below. The slope of the curve for median age of death shows no pronounced turn upwards following 1996 — even though the annual numbers of deaths decreased by more than half between 1994 and 1998. The somewhat steeper increase in median age of death from 1997 to 1999 and the parallel sharper increase in median age of AIDS diagnosis are both artefacts stemming from re-calculation of numbers under a revised International Diagnostic Code, see asterisked footnote to Table 2. The other slight discontinuity in the curve, around 1993, reflects the CDC’s revised definition of AIDS to include asymptomatic HIV-positive people with low CD4 counts.

Figure 1

The uppermost curve, the interval between median age of diagnosis and median age of death underscores that over the whole course of the AIDS era, no episode brought a significant increase in median age of death, other than the drastic expansion of definition in 1992-93. (Of course, the difference between the median ages for diagnosis and death in any given year cannot be equated with the interval between diagnosis and death for any given individual; the significant point in Figure 1 is just that median ages have changed at a gradual and almost constant rate from the very beginning of the AIDS era. HAART changed the death rate dramatically, but not the ages at which people died.)

This constitutes a major conundrum, a paradox: If HAART has extended life-spans by the claimed amounts, then why has not the median age of death increased dramatically? Why were so many AIDS patients still dying around age 45 in 2004?

The resolution of this conundrum is that the median ages of death are based on actually recorded deaths, whereas the claimed benefits of HAART were calculated on the basis of models incorporating many assumptions about the course of “HIV disease” and relying on contemporaneous death-rates [Science Studies 103: Science, Truth, Public Policy — What the CDC should know but doesn’t, 4 September 2008; CDC’s “model” assumptions (Science Studies 103a), 6 September 2008].

The numbers for total AIDS cases and for deaths, shown graphically in Figure 1, are listed in Table 3. There, column III shows the numbers of survivors in any given year, calculated from the difference between cases and deaths in earlier years plus new cases in the given year. Column IV has the percentage of survivors who died each year.

Table 3
Total AIDS cases, deaths, and
survivors “living with HIV/AIDS”,

From 1996 to 1997, the annual numbers of deaths halved, and of course the percentage of deaths among survivors also halved. Since 1997, only between 2.8 and 5.7% of living “HIV/AIDS” patients have been dying annually, which is in keeping with the claims of life-saving benefits made for HAART on the basis of death rates and computer models. But that conflicts with the age distribution of deaths, which has remained without major change during those same years.

If AIDS patients are now enjoying a virtually normal life-span, who are the people still dying at median age 45? If HAART is saving lives, why aren’t those lives longer?

The reason is that testing “HIV-positive” is actually irrelevant to the cause of death. It does not indicate infection by a cause of illness, it is an indicator analogous to fever. Many conditions may stimulate a positive “HIV” test: vaccination against flu or tetanus, for example; or tuberculosis; or drug abuse; or pregnancy; and many more (Christine Johnson, “Whose antibodies are they anyway? Factors known to cause false positive HIV antibody test results”, Continuum 4 (#3, Sept./Oct. 1996).

The likelihood that any given individual exposed to one of those conditions will actually test positive seems to correlate with the seriousness of the challenge to health; and it varies in a predictable manner with age, sex, and race (The Origin, Persistence and Failings of HIV/AIDS Theory). In any group of people, those who test “HIV-positive” are more likely to be or to become ill, so they are also more likely to die than those who do not test positive: just as in any group of people, those who have a fever are more likely to be ill and to die than those who do not have a fever. Also, of course, a fever does not necessarily presage death, nor does “HIV-positive” necessarily presage death; and in any group of people, some will die who never tested positive or who never had a fever. There’s a strong correlation between illness, death, and fever, but it’s not an inevitable one and fever is not the causative agent; there’s a strong correlation between illness, death, and “HIV-positive”, but it’s not an inevitable one and “HIV” is not the causative agent.

So: Among people “living with HIV/AIDS”, those who happen to die in any given year are simply ones whose “HIV-positive” status was associated with some actually life-threatening illness; and their ages were distributed just as ages are distributed in any group of “HIV-positive” people, with a median age at around 40, with minor variations depending on race and sex. For example, in 2000, there were more than 350,000 people “living with HIV/AIDS” (Table 3) whose median age was somewhere around 39.9 (Table 2: 39.9 was the median age of new diagnoses in that year. Survivors from the previous year , when the median age had been 39.4, would have had a median age — one year later — somewhere between 39.4 and 40.4; not as much as 40.4, because those dying in 1999 had a higher median age than those who didn’t die.) Of the 350,000 in 2000 with median age 39.9, 3.9% (14,457, Table 3) died; and the median age of those dying was 42.7. It’s only to be expected, of course, that — among any group of people at all — those who die have a somewhat higher average age than those who don’t die in that year.

The rate of death among “HIV/AIDS” patients declined markedly from 1987 to 1992 simply because “HIV/AIDS” was being increasingly defined to include illnesses less life-threatening than the original AIDS diseases of Kaposi’s sarcoma and established opportunistic fungal infections. Another sharp drop in death rates came after 1992 when people who were not even ill came to be classed as “HIV/AIDS” patients and comprised about 70% of such patients. The last sudden drop in death rates, with the introduction of HAART in 1996, resulted not from any lifesaving benefit of HAART but because the latter superseded the earlier, much more toxic, high-dose regimens of AZT. The supposed benefits of HAART are to decrease viral load and allow CD4 counts to rise; but these effects come slowly and cannot explain a sudden improvement in clinical condition sufficient to bring a halving of deaths from one year to the next; on the other hand, stopping the administration of a highly toxic substance can certainly bring numbers of deaths down immediately. These data indicate, therefore, that something like half (at least) of “HIV/AIDS” deaths from 1987 through 1996 — some 150,000 — are attributable to the toxicity of AZT.

Through all those drastic as well as slower changes in death rates, among those “HIV/AIDS patients” who died for any one of a large variety of reasons, the median age of the “HIV-positive” ones remained about the same as it had always been. “HIV/AIDS” patients are not living longer despite the change in death rate from an annual 60% or more to 3% or less.

As I said in a previous post [How “AIDS Deaths” and “HIV Infections” Vary with Age — and WHY, 15 September 2008], this paradox follows “from the manner in which HIV tests were designed and from the fact that AIDS was defined in terms of ‘HIV’”. The genesis of the tests has been described lucidly by Neville Hodgkinson (“HIV diagnosis: a ludicrous case of circular reasoning”, The Business, 16/17 May 2004, pp 1 and 4; similar in “The circular reasoning scandal of HIV testing”, thebusinessonline, 21 May 2006):

“It never proved possible to validate the [HIV] tests by culturing, purifying and analysing particles of the purported virus from patients who test positive, then demonstrating that these are not present in patients who test negative. This was despite heroic efforts to make the virus reveal itself in patients with Aids [sic, British usage] or at risk of Aids, in which their immune cells were stimulated for weeks in laboratory cultures using a variety of agents.
After the cells had been activated in this way, HIV pioneers found some 30 proteins in filtered material that gathered at a density characteristic of retroviruses. They attributed some of these to various parts of the virus. But they never demonstrated that these so-called ‘HIV antigens’ belonged to a new retrovirus.
So, out of the 30 proteins, how did they select the ones to be defined as being from HIV? The answer is shocking, and goes to the root of what is probably the biggest scandal in medical history. They selected those that were most reactive with antibodies in blood samples from Aids patients and those at risk of Aids.
This means that ‘HIV’ antigens are defined as such not on the basis of being shown to belong to HIV, but on the basis that they react with antibodies in Aids patients. Aids patients are then diagnosed as being infected with HIV on the basis that they have antibodies which react with those same antigens. The reasoning is circular.”

“HIV” tests were created to react most strongly to substances present in the sera of very ill gay men whose average age was in the late 30s (Michelle Cochrane, When AIDS began: San Francisco and the making of an epidemic, Routledge, 2004; cited at pp. 188-92 in The Origin, Persistence and Failings of HIV/AIDS Theory). That’s why people who are in some manner health-challenged are more likely than others to test “HIV-positive”, especially if they are aged around 40. Evidently the particular molecular species picked up by “HIV” tests are generated most prolifically around age 40, especially under the stimulation of various forms and degrees of physiological stress. That’s why the median ages for testing “HIV-positive” and for being diagnosed with AIDS (criterion: positive HIV test) and for dying from HIV/AIDS  (criterion: positive HIV test) are all the same, in the range 35-45.

Perhaps some of what “HIV” tests detect are so-called “stress” or “heat-shock” proteins. That gay men so often test “HIV-positive” might have to do with molecular species associated with “leaky gut syndrome” or other consequences of intestinal dysbiosis [What really caused AIDS: slicing through the Gordian knot, 20 February 2008].

Those are speculations, of course. What is not speculative, however, is that HAART does not prolong life* even as it lowers death rates. It is also clear that testing “HIV-positive” is no more than an indicator of some form of physiological challenge, not necessarily infection by a pathogen and specifically not infection by a retrovirus that destroys the human immune system.

Even as it is obvious that HAART does not prolong life on the average, there are reliable testimonies that individuals have experienced clinical improvement on HAART, often dramatic and immediate. But, again, such immediate benefit cannot be the result of antiretroviral action, and likely reflects an antibiotic or anti-inflammatory effect, as suggested by Dr. Juliane Sacher [Alternative treatments for AIDS, 25 February 2008].

Posted in antiretroviral drugs, HIV and race, HIV as stress, HIV does not cause AIDS, HIV tests, HIV varies with age, HIV/AIDS numbers | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | 5 Comments »

HIV/AIDS SCAM: Have antiretroviral drugs saved 3 million life-years?

Posted by Henry Bauer on 2008/07/06

In the previous post [Antiretroviral therapy has SAVED 3 MILLION life-years, 1 July 2008], I showed that the impression conveyed by “millions” is misleading. The claim actually amounts to an estimate that HAART has saved, at an annual cost of about $20 billion, only about 13% of AIDS victims, in other words about 1 in 8, which is hardly what’s implied by the commonly used description of HAART as “lifesaving”.

I referred also in that earlier post to “dishonesty” in the Walensky et al. article. That charge reflects the fact that only a by-the-way sentence on the fourth page of the article modifies drastically the claim, made in the Abstract, of “at least 3.0 million” life-years saved: “Of these, 1,184,851 years have already been realized, and 1,629,041 years are being accrued by current patients”. The claimed 3 million turns out to be less than 1.2 million! Yet that is once again fudged or masked by the last sentence of the article: “Ten years after the introduction of potent combination ART, at least 3 million years of life have been saved in the United States” [emphasis added]. Counting projected future savings as already in hand might not survive an independent audit.

Repeating the calculations in the earlier post with the lower figure of 1.2 million of actually realized savings, we find that there were saved by 2003 not 13% of patients but only 6%, at expenditure of more than $180,000 per saved life-year, or $12.5 million per life; and our productivity in GDP terms then represents a measly return of 0.36% on this human capital. Such are the numbers that Fauci apparently believes to justify current expenditure on HIV/AIDS. One can be sure, moreover, that the computer model was designed and the calculations made with a view to presenting as rosy a picture as possible. If this is the best they can come up with, then it’s time to stop talking about HIV/AIDS as a manageable, chronic but not fatal disease.

Not only is the claimed benefit of treatment much less than impressive, the claim actually lacks any solid foundation whatsoever. It relies on a computer model that makes a number of unjustifiable assumptions, and it ignores such central issues as the acknowledged toxicity of the antiretroviral treatment as well as how the definition of AIDS has changed, and thereby the health-state of people being treated.

Here is the essence of the Walensky article: “The Cost-Effectiveness of Preventing AIDS Complications (CEPAC) model was used to estimate per-person survival benefits. CEPAC is a widely published computer-based state-transition simulation model of HIV disease that incorporates CD4 cell count; HIV RNA level; ART efficacy; OI incidence, treatment, and prophylaxis; and other important clinical information [16–18, 21]. “State transition” means that the model characterizes the progression of disease in an individual patient as a sequence of transitions from one ‘health state’ to another. . . . In the model, the level of HIV RNA determines the rate of CD4 cell count decline, and the absolute CD4 cell count governs the monthly risk of OIs and death”.
One hardly needs to read any further, given that Rodriguez et al. (JAMA 296 [2006], 1498-1506) found a lack of correlation between “HIV RNA level”—otherwise known as viral load—and the rate of CD4 decline. This fact alone would be enough to vitiate the model; but there are also no valid studies of ART efficacy using untreated controls. As to prophylaxis of opportunistic infections, more is said below.

Walensky et al. considered “6 distinct eras of HIV/AIDS treatment from 1989 to 2003”. But about 50,000 AIDS deaths had already been reported up to 1989 (CDC 1990), about 35,000 of those during the AZT monotherapy years of 1987 and 1988. Some (or most or perhaps even all) of those deaths were caused or hastened by the AZT, and those lost life-years should surely be subtracted from the savings calculated from 1989 on, since HAART typically incorporates AZT or an analog of it, albeit at much lower doses than in the monotherapy era. Instead, Walensky et al. apparently seek to hide AZT toxicity by saying that “we excluded the early benefits of antiretroviral mono- and dual-drug therapy when survival benefits were more limited”, a fine illustration of double-speak: “more limited benefits” here stands for “no benefit, just caused harm”.

The first era commences with “prophylaxis for Pneumocystis jiroveci pneumonia (PCP) starting in 1989”, ignoring that Michael Callen and Josef Sonnabend had pioneered prophylaxis against PCP in AIDS victims years earlier. Callen cites data from the Centers for Disease Control and Prevention that more than 30,000 people had died of PCP by February 1989 even though the possibility of prophylaxis had been known since 1977. Callen himself had urged Fauci in May 1987 to recommend prophylaxis, but Fauci refused; nearly 17,000 PCP deaths occurred between May 1987 and February 1989 (pp. 30-31 in Michael Callen, Surviving AIDS, HarperCollins 1990). That is in direct contradiction to the claim that “88% of eligible patients in the pre-ART era were receiving OI [opportunistic infection, includes PCP] prophylaxis” (Walensky et al., p.12). How many of those 30,000 or 17,000 PCP deaths should be subtracted from Walensky’s 3 million — or actually 1.2 million — saved years of life? 30,000 lives lost to PCP, after all, already represent more than 2 million life-years, and even 17,000 lives amount to over a million-and-a-quarter life-years, either of which would wipe out entirely all the life-years claimed to have been saved between 1989 and 2003.

Walensky et al. cite an estimate that only 57% of known “HIV-positive” people are receiving treatment, and they assert that additional life-year-savings would result if more were being treated. But how many of the non-treated are avoiding antiretroviral drugs by choice? Certainly among gay men, knowledge of the fearsome “side”-effects of antiretroviral drugs has been widespread for two decades. Moreover, any reader of the official Treatment Guidelines learns that “In the era of combination antiretroviral therapy, several large observational studies have indicated that the risk of several non-AIDS-defining conditions, including cardiovascular diseases, liver-related events, renal disease, and certain non-AIDS malignancies . . . is greater than the risk for AIDS”. How then could Walensky et al. legitimately ignore these toxicities, as they do: “The analysis did not account for later ART-related toxicities that may result in, for example, cardiac disease or diabetes”. They wave aside the iatrogenic harm from ART even further by opining that “hyperlipidemia reduces overall life expectancy by ~1 month”. When your doctor tells you that your cholesterol is too high and that you should begin a lifelong course of expensive statin drugs — whose deleterious “side” effects also call for regular doses of Coenzyme Q10, which few doctors will tell you, however —, try responding that you have it on good authority that the potential benefit of conquering hyperlipidemia is only about 1 month of extra life. Let me know what your doctor says to that.


Noted by Walensky et al. is that “after 1992, ~70% of new AIDS diagnoses were made according to a CD4 cell count criterion of <200 cells/mm3 alone”. This criterion for an AIDS diagnosis is unique to the United States, and patients thus diagnosed may display no symptoms of illness. Thus up to 70% of “AIDS” patients receiving antiretroviral drugs in the United States since 1993 have been clinically healthy when they begin “treatment”. It would then be hardly surprising that survival rates increased from the years before 1993 when this CD4-count criterion was introduced, for initially healthy people will surely survive toxic drugs longer than people who are already ill: “projected per-person survival after an AIDS diagnosis increased from 19 months (1.6 years) in the absence of treatment to 179 months (14.9 years) by 2003, a gain of 160 months (13.3 years)” [emphasis added]. The all-knowing computer model can apparently be sure already in 2003 that patients will survive on average into 2018. But even this projection hardly justifies the assertion that AIDS is now “a highly treatable chronic condition”, given that even by 2004 — 8 years into the “lifesaving” HAART era — most deaths from “HIV disease” were still occurring among people around 40 years of age, just as two decades earlier [Table 42, p. 236, in “National Center for Health Statistics: Health, United States, 2007 with Chartbook on Trends in the Health of Americans”, Hyattsville, MD, 2007; see “HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008].

Puzzling is the statement that “Mean per-child survival gains for the averted infections ranged from 60.5 years if the child was born before 1996 (before combination ART) to 45.8 years during 1996-1999, when combination ART was available”. If ART is better, why is the survival gain from it only ¾ of the earlier survival gain from pre-ART prophylaxis of opportunistic infections?


It also remains for me a continuing mystery that so many AIDS researchers, reviewers of HIV/AIDS manuscripts, and editors of journals that publish this material are so lacking in elementary numeracy as to pepper their articles with numbers like “832,179 years in ART 3”, “2,813,892” years saved, and so on. Numbers no less than words should convey meaning. The only thing conveyed clearly by “2,813,892” is that the writers take computer outputs as sacrosanct and don’t think about what the numbers mean. Those extra digits are not only meaningless, they positively distract the reader, making necessary a mental rounding-off to recognize that the substantive claim is “about 2.8 million”; not many people, after all, are used to digesting 7-digit numbers and savoring their significance. In the Walensky et al. article, the mystery of this abusive mathematical incompetence is only deepened by the fact that the authors’ affiliations include departments of epidemiology and biostatistics.


Walensky et al. “employed a model-based approach, conducting repeated analyses to explore the clinical consequences of alternative patient-care-innovation pathways”. The whole article deals not with actual patients but with “hypothetical patients”. This fulfills the suggestion, reported in a previous post, that one no longer needs human beings for clinical studies, computers can conveniently substitute [VIRTUAL HIV/AIDS RESEARCH AND TREATMENT, 17 June 2008]. The most convenient thing about this, of course, is that it’s much easier to get the results you want from a computer model you have yourself designed than from observations of real people.

Here’s the point to bear in mind whenever the gurus parade the outputs of their computer models:
A computer model can be guaranteed to mimic reality faithfully only if everything about that reality is already known in every detail. But if that is so, then one doesn’t need a computer model. Computer models are experiments carried out on surrogates of reality, surrogates that are unavoidably simplified and based on assumptions about reality. In the Walensky et al. case, the model incorporates assumptions about what happens to a person with a given viral load and CD4 count under no treatment, and what happens to individuals with given viral loads and CD4 counts under a variety of treatment regimens: all of which are based on guesses, because clinical trials with proper controls have never been carried out to determine properly the parameters needed for such a model. Moreover, as earlier mentioned, the article by Rodriguez et al. found no correlation between “viral load” and subsequent decline in CD4 counts. Further, the article ignores the well established phenomenon of “long-term non-progressors” or “elite controllers”, individuals who demonstrate that being “HIV-positive” does not necessarily lead to destruction of the immune system, illness, and death. How could the fates of non-treated “patients” be modeled when this phenomenon is ignored? When it is not even known what proportion of people are potentially elite controllers?

The outputs of this model deserve no credence whatsoever. The claim of more than 3 million saved life-years is utterly bogus. Even were it not bogus, it would reveal the claimed benefits of antiretroviral therapy to be at best marginal and procured at egregiously excessive cost.

Posted in antiretroviral drugs, clinical trials, experts, Funds for HIV/AIDS, HIV absurdities, HIV/AIDS numbers | Tagged: , , , , , , , , , , , , , | 4 Comments »


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