HIV/AIDS Skepticism

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

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.

35 Responses to “Poison in South Africa”

  1. An “exercise in propaganda and politics”

    Isn’t that what it’s all become? Every day their camp is just filled with this type of illustrious achievement and the journals, well, they just think it’s the cat’s meow. I often wonder how much money these guys receive for their so valued research.

  2. Martin said

    Hi Dr. Bauer, I just saw the following article in the Boston Globe today “Earlier AIDS treatement lengthens lives, study finds”.
    It goes right along what you’ve been talking about. GIGO

  3. Nick Naylor said

    Congratulations once again, Henry, for providing scrutiny of more meaningless quantitation by AIDS Inc. — the use of mathematical models with made up parameters.

    The latest study in this pathetic series — by those who don’t even care that their prostitution to Big Pharma has been so exposed — represents a new offensive by the medical totalitarians.

    The New York Times has just “reported” another set of scurrilous attacks on Mbeki: http://www.nytimes. com/2008/ 11/26/world/ africa/26aids. html?_r=1&ei=5070&emc=eta1&pagewanted=all.

    For what it’s worth, I will send them excerpts from your write-up plus commentary on the wretched state of “epidemiology”.

    And yes, it starts with the scam of Montagnier and Gallo on HTLVIII/LAV “patient isolates”.

  4. Henry Bauer said


    Thank you!

    Re Big Pharma: Among the TV ads that I haven’t avoided is one that offers help to people who can’t afford their prescriptions, help said to be from pharmaceutical research companies, a not-too-subtle reminder that Big Pharma is all about doing research to make us all better. Obviously not their fault when things get approved after too short trials, or for no good reason, like say the Gardasil anti-cervical-cancer vaccine

  5. CathyVM said

    “Today, not only are we working to discover the next new medicine [blockbuster – so we can laugh all the way to the bank], but we’re also working to help make healthcare a more meaningful, more personal experience for patients [and generally much more expensive]. The key to this goal is empowerment [brainwashing]. By empowering [brainwashing] patients with information [DTC advertising propaganda], and providing access to medicines [dumping dangerous, unproven medicines on the market] and support systems [cute detailers with big breasts and shiny hair], we can help patients make better informed [our drug, our drug, our drug] choices about their care [iatrogenic damage], and ultimately help them lead healthier lives [hahahahahahaha].”

  6. CathyVM said

    But wait, there’s more…
    We want to discover [misappropriate compounds developed using tax dollars], develop [once the tax dollars are spent and we think it might fly] and successfully market [brainwash doctors and the public] innovative [me-too drugs that offer nothing over older drugs apart from risk of death] products to prevent and cure diseases [umm, name me one drug that prevents or cures anything], to ease [cause] suffering and to enhance [detract from while lining our own pockets] the quality of life [slow death].

    At Pfizer, we’re inspired [motivated by greed] by a single goal [picking your pocket]: your [ill] health. That’s why we’re dedicated to developing new [but strangely similar to existing drugs], safe [well nothing showed up in very short-term trials and if it did it’s nothing to do with our drugs] medicines [poisons] to prevent and treat [yeah, right] the world’s most serious diseases. And why we are making them available to the people who need them most [let’s flood Africa with our toxic HIV drugs so we can look philanthropic while committing genocide]. We believe that from progress [in financial markets] comes hope [of more filthy profits] and the promise of a healthier world [no comment would do this BS justice].

  7. Henry Bauer said


    Can you imagine what it’s like to believe that you have to earn your living writing — “creating” — that stuff?
    The British consumption tax is called VAT, “value added tax”, on the presumption that “value” is added at every stage of production of goods and services. But added commercial value seems more and more to correlate with DECREASED social value — at least in so-called “developed” or “First World” countries.

  8. CathyVM said

    Well for 2 years I earned my living reading and reporting on such bilge. Years later I still have a bad taste in my mouth.

  9. sadunkal said

    Hi Prof. Bauer, I got good news: I’m going to point out a mistake of yours that I perceive. 🙂

    I had a little discussion with Snout (whoever that is) and Chris Noble elsewhere, and Snout asked a question in regard to your point no.1 above. It made sense to me, I tried to persuade Snout to come here and post the comment himself but he wasn’t willing to do that, so I decided to do it myself for various reasons:

    In that Lancet study, when they say “but such improvement has not translated into a decrease in mortality”, were they comparing HAART c1995-6 with HAART c2002-3, or HAART with no HAART?

    I think Snout is right about this. The phrase “but such improvement has not translated into a decrease in mortality” seems to mean only that HAART 2002 isn’t saving more lives than HAART 1996. But you seem to have interpreted it in a way that it means “HAART is not better than no HAART”. As much as that may also be true for many patients, I don’t think that’s what was meant in that paper.

    What do you think about this?

    And for transparency, if you’re interested you can read the whole discussion here:

    It’s pretty ugly and unscientific in general, but if you can ignore all the excess of emotions, there’s also a little food for thought, I guess. I hope it won’t bother you too much.

  10. Henry Bauer said



    The Lancet 2006 article points out that suppression of viral load did not result in decreased mortality. Yes, they do compare 1995-96 HAART to later HAART, but the conclusion remains: “the virological response after starting HAART has improved steadily since 1996. However, there was no corresponding decrease in the rates of AIDS, or death, up to 1 year of follow-up.” In other words, HAART suppresses virus, with increasing success over the years, but that increasing success doesn’t translate into clinical benefit.

    Following that statement comes:
    “Conversely, there was some evidence for an increase in the rate of AIDS in the most recent period”.

    In other words, more recent HAART, or being on HAART for a longer period of time, increases “AIDS” events. The authors suggest this might be owing to a change in the patient population:

    “The discrepancy between the clear improvement we recorded for virological response and the apparently worsening rates of clinical progression might be related to the change in the demographic characteristics of study participants, with an increasing number of patients from areas with a high incidence of tuberculosis.

    However, the NIH Treatment Guidelines admit that HAART causes the majority of adverse events in treated patients:
    “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 [97-102] is greater than the risk for AIDS in persons with CD4 T-cell counts >200 cells/mm3; the risk for these events increases progressively as the CD4 T-cell count decreases from 350 to 200 cells/mm3.”

    I don’t think I’m misquoting the literature here.

    Thanks for the link and invitation, but I don’t participate in discussions where people sling personal insults around, and I don’t read such stuff. It’s simply a waste of time for me, I’ve seen far too much of it over the years in such matters.

  11. sadunkal said

    Hmmm…Interesting. I don’t have the full paper, so I’m speculating a bit. But I still perceive your statement in regard to the that lancet study “…in other words, no life-saving benefit at all.” as a little problematic. Wouldn’t it represent the study more accurately if you’d say “in other words, decrease in viral load brings no life-saving benefit at all.”? And maybe add that “Recently even worsening rates of clinical progression was observed despite the the “improvement” in virological response.”?

    Sure HAART might statistically have “no life-saving benefit at all”, but I don’t think that conclusion can be reached based solely on that study. For those who believe in the HIV/AIDS hypothesis, despite all the adverse effects, these drugs are still allowing people to run away from certain death for a period of time. So they won’t interpret the paper as someone who doesn’t believe in it and they’ll be able to claim that you’re misrepresenting the study, as they already do obviously.

    P.S. To clarify; I’m not saying that you misquoted it, but you seem to have taken it a little out of context and this makes it easier for your readers to misunderstand what the authors actually meant.

    P.P.S. And of course for someone who doesn’t read the comments it still won’t be clear that the conclusion was in regard to a comparison between 1995 and 2002 HAART if the text above remains as it is.

    • Henry Bauer said


      I’ve learned that there is no possible way to defende oneself against misinterpretation, be it deliberate or through lack of understanding. Anyone who is seriously interested in the issue must read the full paper that is under discussion. If Snout or Noble won’t do that, then they’re not seriously interested in the substance of the issue. If they’ve read the paper and want to nitpick time periods instead of addressing the critical substantive point, then they aren’t seriously interested in the substantive issue.

      To my mind, the critical point is, does HAART save lives? The article reports that it doesn’t, if anything, it does the opposite, even though it is successful “virologically” — and that fact shows at the same time that it isn’t the “virus” that harms health.

  12. Sabine Kalitzkus said

    “I don’t have the full paper, so I’m speculating a bit. But I still perceive your statement … as a little problematic. Wouldn’t it represent the study more accurately…”


    Please read the full paper. How can you perceive a statement as “problematic”, and how do you know, what would represent the study “more accurately”, if you haven’t read the paper?

  13. sadunkal said

    So is your logic that since improvements in virological response don’t translate into a decrease in mortality, and since HAART is supposed work through its anti-retroviral properties, it can’t be said that it ever had any life-saving benefits to begin with?

    This sounds like it makes sense to me. But if that’s your logic, one must also consider the antibiotic effects of HAART. So even if the drugs aren’t working the way they’re supposed to work, they may still have some life-saving benefits in comparison to a placebo. I think it’s unlikely, but it’s impossible to say without a placebo study or without a close examination of the antibiotic effects vs. adverse effects. Wouldn’t you agree?

    • Henry Bauer said


      You’ve grasped my point.

      As to possible antibiotic effect, what has that got to do with an immunedeficiency-causing virus? There are specific antibiotics available for specific bacterial, fungal, and parasitic illnesses, antibiotics that have far fewer and less serious “side” effects than antiretrovirals do. HAART is supposed to be specifically targeting a retrovirus that supposedly kills the immune system. Apparently suppressing the virus doesn’t go hand in hand with making patients better.

      Please read my blogs referring to Juliane Sacher, who treats AIDS patients successfully with alternative or complementary treatments. As a last resort, she sometimes uses antiretrovirals for a brief period in the expectation that their all-purpose cell-killing action may target unrecognized inflammation.

  14. CathyVM said

    Also remember that for some time in the 60’s and 70’s they tried to develop synthetic antibiotics with “anti-viral” activity. The first semi-synthetic antibiotic was Rapamycin, the side effects of which read like a laundry list of “AIDS” manifestations, and which was re-branded in the early 80’s as Sirolimus due to its profound ability to induce immune suppression thereby proving its “usefulness” in preventing graft/transplant rejection.
    How many homosexual men in SF and NY were taking this antibiotic long-term and prophylactically?
    How many received it as treatment for STDs?
    And where did the dread syphilis go anyhow?

  15. Köpek Burun said

    Ms CathyVM is making an interesting thought about the macrolide drug Rapamycin (Rapamune or Sirolimus) which has antifungal as well as anti-rejection properties, however this drug was not ever used by homosexual men in SF and NY as a treatment or prophylaxis for STDs during the 1970s and 1980s.

    It was only approved for humans uses since 1999, and for the uses as a transplant antirejection drug, not as an antibiotic or antifungal. It also has some promising uses in eluting stents for treatment of sclerotic arterial disease, and for the treatment of several other diseases.

  16. Sadun Kal said

    This text by Neville Hodgkinson already covers what we so far talked about:

    Click to access AntiHIVdrugsFail.pdf

    “As to possible antibiotic effect, what has that got to do with an immunedeficiency-causing virus? There are specific antibiotics available…”

    I’m not defending HAART. But talking from a technical perspective, if it has antibiotic effects then it has antibiotic effects. And these effects may somehow really be saving some lives in a way which would be statistically significant, even if they are not as good as they would be with specific antibiotics. I think it’s unlikely, but not impossible.

    And the mortality rates didn’t get worse either despite “changes in patient demographics, patients receiving treatment too late to get the full benefit, more co-infection with other diseases etc.” as reported in the study as an explanation. I think this gives that possibility I mentioned above a higher chance: It would mean that the beneficial side-effects made up for the worse conditions. But that’s highly speculative since it may also simply be that the adverse effects of HAART has gotten lesser over the years.

    Generally saying that they have “no life-saving benefit at all” is a little too certain without a placebo study in my opinion, which is unfortunately said to be unethical. I suspect even telling people that they don’t have AIDS would work as an effective placebo by the way, as telling people they do have AIDS is the worst mass Nocebo mankind will ever have created, possibly.

    • Henry Bauer said


      Re your citing the Hodgkinson paper: I still don’t understand your point. The orthodox position is that HAART works because it suppresses virus. The data show that is not the case. Virus is apparently suppressed but people don’t live longer.

      It doesn’t need a placebo study to note that the median age of death from “HIV disease” has not increased during the HAART era in a manner that demonstrates signficant life extension. Look at Table 2 and Figure 1 in “HAART saves lives — but doesn’t prolong them!?”, 17 September 2008,’t-prolong-them/
      Note that the average time between new diagnoses and death shows no significant break when HAART came into use, no break anywhere near enough to warrant the claim of extending life by more than a decade. (I’ve recently done more calculations, based on Table 2 to calculate the age distributions of PWAs, and those median ages show this even more convincingly.)

      It’s just not relevant, to wonder about antibiotic effects of HAART. That’s one of the many tasks for the future, when it comes to looking into what specific illnesses some HIV+ people might have (had) and what the actual specific causes were for the so-called “HIV disease” deaths. I said HAART has no lifesaving benefits at all, in the context of HIV/AIDS theory. Please don’t pick up bad habits from Snout et al. 😉

  17. Sadun Kal said

    Apart from that, Chris Noble sent me this link as a contradictory example:

    It says this:

    “In a failure-rate model, increases in the intensity of antiretroviral therapy (classified as none, monotherapy, combination therapy without a protease inhibitor, and combination therapy with a protease inhibitor) were associated with stepwise reductions in morbidity and mortality.”

    I don’t know what to think of that. But let me present that paper with this:

    Again, speculations… What do you think?

    • Henry Bauer said

      Sadun Kal:

      The citation sent by Noble is from 1998 and is based on a model, using data obtained during a mere two years after HAART was introduced. It has been long superseded.

      Many thanks for the link to the fascinating essay by Richard Smith,

      Yes indeed, conflicts of interest pervade what is published about drugs. References 2 and 3 given by Smith are very much worth reading. It is nowadays very hazardous to health, to use any drug that hasn’t been on the market for several years, because drugs get approved on the basis of insufficiently long and rigorous trials, and one discovers the sometimes fatal “side” effects only through the fallible process of reporting from individual doctors and hospitals.

  18. Macdonald said

    Look Sadun, you’ve been doing this long enough to know how to think your way out of Noble’s and Snout’s “challenges”, or at least long enough to distinguish the real challenges from fruitless nitpicking.

    Nothing you or your new friends are coming up with has not been answered here several times. Try the search function.

    There are hundreds of thousands of HIV papers; does it really throw you into confusion that Noble et al. can come up with a couple that seem to support the idea that ARVs are beneficial? Well, let me shock and awe you then; most of the published papers will seem to support the notion that ARVs are life-saving or whatever. If you don’t learn for yourself how to look behind and beyond that, Prof. Bauer will be spending all his time delivering the same answers to you in different contexts.

    If Snout and Noble can come up with an intelligent critique of Prof. Bauer’s point about the unchanged median age from infection to death in “the age of HAART”, let’s hear it, otherwise tell them to go shilling on Todd DeShong’s blog.

  19. Sadun Kal said

    I found that essay by Smith while reading this:

    And I think it’s interesting that the person who says “Journals have devolved into information laundering operations for the pharmaceutical industry” is also the only journal editor who had the guts to confront HIV/AIDS critics in a debate, where he also made this confession:

    “I’m afraid to say that some of my editorial colleagues on other journals have operated censorship, very openly and have admitted they will not publish his point of view. Indeed, they will go as far as they can to publish points of view that directly contradict Dr. Duesberg.”

    Richard Horton is the editor of Lancet. As far as I know he was the only editor who allowed himself to get seriously involved in all this, the other editors pretended that there never was anything to debate. And Horton was also the focus of Serge Lang’s criticisms for his unscientific approach to HIV/AIDS debate. Imagine if someone as biased and unscientific as Horton — at least in the past in regard to HIV/AIDS — can make such stunning confessions, what would the real, completely dishonest editors say if they were to tell the truth? It would probably be extremely scandalous.

    There is also this one there, which I didn’t yet read:

    Back to HAART; my point was irrelevant to what the orthodox view is, it’s just about being true to what HAART may be capable of in the real world with real people. But when you say “I said HAART has no lifesaving benefits at all, in the context of HIV/AIDS theory” then I don’t have a reason to disagree, I got nothing to criticize — except that it’s not put that clear in the above blog post.

    And I must confess that I have a hard time grasping what and how those tables and figures can tell us about what HAART does. I have a lack of knowledge, understanding and parallel to that also a lack of trust for the reliability of your conclusions. But I have to inform myself before I begin to talk about that — i.e. read your book :)-, which I might never find enough time for. So I just shut up for now. 😀

    Snout or Chris Noble are welcome to put forward any scientific arguments themselves.

    • Henry Bauer said


      “I have a hard time grasping what and how those tables and figures can tell us about what HAART does. I have a lack of knowledge, understanding and parallel to that also a lack of trust for the reliability of your conclusions.”

      The only satisfactory thing for you is to grapple with the data until you DO get a feel for what they mean. Then you will have a chance to compare YOUR CONCLUSIONS with mine. Forgive me if I sound like the former teacher that I am: I don’t want anyone to accept what I say just because I say it. That leaves you helpless when others nitpick or argue. The whole purpose of learning about something is to make the knowledge YOUR OWN.

      Of course it’s hard. I spent many months unable to believe what I was seeing in the HIV data that eventually got into my book, and also finding no flaws, and being unable to find anyone willing to discuss it with me in detail. But there’s nothing magical about these numbers, you just have to become familiar with what they mean and then use common sense.

  20. Sadun,

    Please read my articles:

    1. United States AIDS Case Fatality Rates 1981-2005

    2. Some Observations on HIV/AIDS Epidemiology

    The severity of the “epidemic” peaked long before HAART came out.


  21. Sadun Kal said

    I agree I agree… I’m just trying to act -and communicate- as unbiased as possible. I don’t want to suddenly find myself as having taken sides at the cost of objectivity one day. We’ve all seen it happen too often.

  22. Sadun Kal said

    By the way, this is not so relevant but the PLoS Journal appears to have really ethical, scientific standards and publish many anti-establishment papers:

    Certain scientists might want to try their chance over there. They also find place in news reports:

    Their open access mentality alone is very praiseworthy in my opinion. I’d say such radical steps will shape the future of science. I personally have the dream that more or less every scientific study will have its own YouTube channel in the future and those who are interested will be able to inspect the process for themselves through videos. That would have certainly stopped Gallo from being able to publish his fraudulent papers, thus save us a lot of trouble.

  23. Köpek Burun said

    Professor Emeritus Bauer, your statement “HAART saves lives — but doesn’t prolong them!?” does indeed sound paradoxical.

    However, in the table 2 that you reproduce in your article by that name, the median age at which people with HIV/AIDS died actually increased from 39.5 years to 45.0 years between 1995 and 2004.

    Furthermore, the percentage of people with AIDS unfortunate enough to die each year during that period fell dramatically. In 1995 there were 43,100 deaths among 200,700 PWAs (21.5%), while in 2004 there were 17,000 deaths among 404,800 PWAs (4.2%). If PWAs had died at the same rate in 2004 as in 1995 there would have been an extra 70,000 deaths that year.

    An increase in median lifespan of 5.5 years for people with HIV/AIDS in 2004 is thus an underestimate for the group as a whole, as it does not include the age of death of people with AIDS who did not die during the period, but could have been expected to based on the 1995 rate of death.

    Any estimate of life expectancy within a group thus needs to consider not only the median age of deaths that occur, but also what is the proportion of the overall group that suffers those deaths.

    If, as is claimed, HAART adds decades to median lifespan then we should not expect median age of death to suddenly increase by decades within the first few years, because you have to live the extra decades before the age of death can be recorded.

    In other words, the deaths recorded in the first few years of HAART are those whose additional survival attributable to HAART are towards the left tail of the distribution curve. Those toward the middle and the right are by definition more likely still alive, and thus are contributing to the “survival with AIDS” statistics, not the “median age of death” statistics.

    If HAART is increasing survival what you would expect to see in the short term is a gradual trend toward increase in the median age of death of those who do actually die, and an increase in the percentage of people who survive.

    This appears to be what the statistics are showing.

    • Henry Bauer said

      K B:

      Please read ‘No HIV “latent period”: dotting i’s and crossing t’s’, 21 September 2008“latent-period”-dotting-i’s-and-crossing-t’s/

      As to the increase in median age from 1995 to 2004, there was also an increase from 1982 to 1995: the former is about 0.6 years per year, the latter only 0.3, but still, there’s something other than HAART bringing about that increase.

      That the number dying fell dramatically applies only to the “step” at 1996/97, then the decrease is rather slow and small.

      I agree that one needs to consider which the people are who are dying. I tried, without success and for some time, to construct a scenario like the one you suggest. It’s rather laborious and has taken me some time to calculate from Table 2 the age distributions of PWAs, i.e. survivors, for each year, but the result was worth the labor, because it turns out that the median ages of people living with AIDS in any given year is within a couple of years of the median age of those who die in that year. In fact, the difference is greater in the early 1990s than it is in earlier years or in the later, HAART, years. If treatment were prolonging life, then the median age of survivors ought to grow steadily while that of those dying remains the same, and lower. Instead, they vary approximately in parallel, with the median age of death higher than that of the survivors.

      Another paradoxical feature of “AIDS” deaths is that the rate is greatest at ages 35-45, and its lower at greater ages as well as at lower ages. This is unlike all other diseases, or all-cause mortality, where the age distribution of deaths is U-shaped or V-shaped: the youngest ones, and also the oldest, succumb more easily to health challenges. With “HIV/AIDS”, adults in the prime years iof life die at a greater rate than younger or older people. That’s off the topic of HAART, of course, but it’s an important fact that speaks against HIV/AIDS theory, and it’s quite obvious in the age distributions in Table 2.

      BTW, the death numbers you cite appear to come from the Division of HIV/AIDS, whereas the data in Table 2 are from the National Center for Health Statistics. The Division publishes “point estimates” derived from their computer model, and differs increasingly over the years with the Center’s numbers which are based on death certificates; see for example “CDC versus CDC: Which Data to Believe?”, 15 August 2008,

      However, this doesn’t affect the points we are discussing, it just changes the magnitude of the changes.

  24. Sadun, you said,

    “I agree I agree… I’m just trying to act -and communicate- as unbiased as possible. I don’t want to suddenly find myself as having taken sides at the cost of objectivity one day. We’ve all seen it happen too often.”

    You still don’t get it yet, do you?? According to “them”, simply by acknowledging the existence of a discussion of the issues, you have already lost your objectivity.


  25. Sadun Kal said

    Haha 😀 I’m afraid I always forget that. It’s hard to get rid of this religious belief in the power of debates after failing to submit myself to years of brainwashing… I have to learn to be more scientific and stop questioning things as soon as possible or I’ll burn in the hell of 21st century Science, tortured forever by evil Galileo and his freaky telescopical minions… Ahem…

  26. Köpek Burun said

    Dear Professor Emeritus Bauer,

    Firstly, thank you for your kind reply. I take it you agree, then, that the median age at which persons diagnosed with AIDS have been dying is increasing each year, and the rate of increase itself showed a marked and more importantly sustained increase from around 1997, averaging 0.67 years annual gain from 97-98 to 03-04, compared with 0.30 years annual gain from 82-83 to 96-97.

    However, my point is not so much that those people dying with AIDS are doing so at a steadily increasing median age, it is that fewer of them are actually dying at all in recent years. It is the latter which is the strongest indicator of increasingly prolonged survival with AIDS, as the group which is actually dying each year (while showing a trend to dying older) represents a smaller and smaller proportion of people with AIDS.

    While it is true that the magnitude of the drop in the death rate in 1996-97 was not followed by drops of similar magnitude in following years, the lower death rate was sustained, and indeed the rate continues to fall, albeit at a lesser pace than around 96-97. For obvious reasons, death rates cannot continue to fall at the same rate they fell between 96-97, otherwise they would soon fall below 0 per cent! Indeed, even if AIDS were completely controllable to the point it made no difference to survival, the death rates would eventually begin to climb again as people entered the ages of natural death from other causes. This upswing has not happened yet.

    It is clear, then, that something happened around 1996-7 to significantly improve the survival of people with AIDS. Whether this was attributable to the introduction of HAART or not, I cannot say on these figures alone, but they are at least consistent with that hypothesis.

    Secondly, thank you also for pointing out your argument about “no HIV latent period”. Again, I think this argument illustrates a similar problem as your argument about calculating survival considering only deaths which have already occurred up to a point in time, rather than all eventual deaths among the cohort.

    In figure 3 of “No HIV latent period: dotting i’s and crossing t’s” you map the age distribution of HIV positive diagnoses with the age distribution of deaths, and seem to be arguing that since there is little difference between the two curves there is no appreciable latent period between HIV diagnosis and death – an apparent statistical absurdity which would be a great surprise to the many people living with an HIV diagnosis, some for many years and even decades.

    However, the while the HIV positive curve includes all diagnoses, the deaths curve includes only an unrepresentative portion of deaths of people represented in the HIV positive curve (assuming that each distribution curve changes little from year to year). If the graph used data to 2005, it would include only the deaths of those people diagnosed in 1985 who survived less than 20 years, those diagnosed in 1995 who survived less than 10 years, those diagnosed in 2000 who survived less than 5, and so on.

    In other words, you are comparing the age distribution of all HIV positive diagnoses with the age distribution of deaths only among a subgroup selected for the worst outcomes. The more recent the diagnosis, the more marked the selection bias for those with the shortest survival, compared to the eventual survival of all those diagnosed in a given year. And all other things being equal, those with the shortest survival will have on average the earliest age of death. Thus, this selection bias pushes the age of death distribution curve to the left relative to a curve which represents the age distribution of all eventual deaths of people represented by an HIV positive diagnosis curve. It also squashes it, which accounts for the narrower width of the death distribution curve relative to the HIV positive diagnosis curve.

    I bring this point up, because I think it illustrates a flaw similar to that which allows you to argue that an only gradual increase in the median age of actual deaths is inconsistent with a major change in survival in the group as a whole.

    A true indication of latency can only be established by taking a cohort where time of seroconversion is known and following that cohort over time. This has been done with numerous cohorts where the time of seroconversion is known, and the median survival of around a decade without antiretroviral therapy has been found repeatedly, with some minor variations associated with age at seroconversion and other factors.

    • Henry Bauer said

      Köpek Burun:

      I didn’t express myself clearly enough in my last response, when I said, “I tried, without success and for some time, to construct a scenario like the one you suggest.” I meant, I tried to think, as you do again, in qualitative terms about cohorts, fractions of cohorts, and so on. The only way to judge whether such speculated expectations are sound or not is to make them quantitative. I have not been able to construct a scenario with actual fractions of earlier cohorts, etc., that fits both HIV/AIDS theory and the actual data on deaths. If you can, I’ll be genuinely interested to see it. For example, you say “people diagnosed in 1985 who survived less than 20 years” — while the facts are that essentially no one diagnosed in 1985 would have survived anywhere near that long — note the mortality rates were 60-70% into the mid-1980s and then decreased to still 35% in 1992.

      ‘No HIV “latent period”: dotting i’s and crossing t’s’ makes a semi-quantitative argument that I still regard as sound, based on the width of the age distributions. That uses the same sort of expectations as you do, that infections and deaths in each cohort have to be represented by distributions, not single numbers (median ages). Recognition of that fact leads inescapably to the conclusion that the age distribution of deaths must be broader than that of infections or diagnoses. The fact is the very opposite.

      For a genuinely quantitative comparison, as I said in my previous response, I’ve at last finished the lengthy calculations of age distributions for cumulative survivors in each year, which is a more suitable comparison with deaths than the new diagnoses are. In either case, though, it isn’t the absolute magnitude of the upward drift in median age of death that matters, but the difference in years between median age of death (= life span) and the median age of the population from which those deaths come. It turns out that the differences between median death-age and median PWA-population-age are even smaller than the differences between new diagnoses and deaths.

      Consider what that means. The life span (= average age of death) in the population of PWAs (people with AIDS) is only a couple of years greater than the average age of the population. That implies that the whole population of PWAs is essentially on the verge of death — yet the death rate is only a few percent! Evidently, what selects for “PWAs” is not what selects for death among PWAs. If the distinction were that those dying had not benefited from HAART, whereas the survivors had, then the median age of survivors should have steadily increased and should have overtaken the average age of death; but there’s no sign of that, the age of death continues to be a little higher than the average age of the population of PWAs.

      In the early 1980s, this conundrum did not exist: average life span was only a few months in excess of average age of PWAs, and death rates were 60+%. But on the early ’80s, the diagnosis of AIDS was based on clinical symptoms, whereas now it’s based on lab tests, positive HIV tests plus CD4 counts. That’s what has produced the paradoxes. People are being diagnosed as having AIDS when they don’t, they just happen to test HIV-positive.

      I realize that I’ve shifted the argument from what HAART does or doesn’t do, to asserting that the death statistics in themselves afford a conundrum that cannot be resolved under HIV/AIDS theory. But the same reasoning can serve to discredit any benefits from HAART.

      I suppose I had better post the results of my calculations, it isn’t fair to refer to them wihtout doing so. It’ll take me a little while still to put in the citations and descriptive text.

  27. Köpek Burun said

    Dear Professor Emeritus Bauer,

    When I said “people diagnosed in 1985 who survived less than 20 years” I was, of course referring to people diagnosed with HIV infection rather than those diagnosed with AIDS. This was in the context, you will recall, of comparing “age of death” curves with “age of HIV positive diagnosis” curves. I apologise if I was unclear about this, as mixing up HIV diagnoses with AIDS diagnoses causes no end of confusion when calculating survival.

    Having said that, I think the principle I outlined above still applies whether you are talking about the age of death distribution among people with HIV or about that distribution among people with AIDS. If you are trying to derive average survival after a diagnosis of AIDS by comparing “age of AIDS diagnosis” curves with “age of death” curves then you must wait until all the people represented in the diagnosis curve have actually died, otherwise you are biasing the age of death distribution curve toward those who died soonest. This bias is most marked when those who actually died are a relatively small proportion of the overall numbers of people living with AIDS.

    The nub of your “conundrum”, therefore, is that your death figures are not complete with respect to any particular “year of diagnosis of AIDS” cohort, except perhaps for those diagnosed with AIDS in the earliest years when long term survival was unlikely, and thus the death distribution figures approach completion. In later years, the proportion surviving since diagnosis till now is much greater, and therefore the age of death figures are far less representative of the cohort as a whole and biased much more to that portion of the cohort that has had the shortest survival. Deaths in this relatively small subgroup, those with the worst outcomes, occur closest to the time of diagnosis. If such relatively poor outcomes are distributed evenly by age through the PWA population, it is not surprising that the age distribution of these earliest deaths would closely follow the age distribution of diagnoses.

    It is for this reason that average or median survival after an AIDS diagnosis cannot be calculated simply by comparing the distribution of age of diagnosis and the distribution of age of whatever deaths have occurred over the same period. A true median survival period can only be calculated by taking a cohort and measuring the actual time until half the members of that cohort have died.

    It is true that it is difficult to compare survival with AIDS between those diagnosed after 1993 compared with before then because of the broadening of the definition of AIDS to include laboratory evidence of immunosuppression as well as diagnoses of opportunistic disease. However, this doesn’t apply to comparisons between 1995 and 2004, as the definition of the diagnosis was the same.

    I look forward to seeing the results of your calculations.

    • Henry Bauer said

      Köpek Burun:

      To repeat: my “dotting i’s…” shows how one can semi-quantitatively compare HIV infection, AIDS diagnosis, and deaths; and the age distributions are simply incompatible with HIV/AIDS theory or benefit from HAART.

      If your “principle” holds up, then all the calculations of HAART benefits — which I have criticized on other grounds — are faulty, because all are based on lowered mortality observed within a few years of beginning HAART, while projecting life extensions of decades.

      On the other hand, if the average time between “diagnosis” and death is only a few years, one would have most of the relevant age distributions already observed. That’s the conundrum. If diagnosis and death both refer validly to a fatal infection, and their median ages are within a few years of one another, then the observed mortality should be very high; and it isn’t, in recent years. It was in the early ’80s, when diagnosis was validly based on clinical symptoms.

      Please wait a day or so until I can post the calculations. They’re important, but as my friend Jack Good likes to say, “The urgent drives out the important”, and I tend to do necessary household chores and answer mail before getting to the important stuff.

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