HIV/AIDS Skepticism

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


Posted by Henry Bauer on 2012/11/10

At first blush, it seems incredible that the international medical-scientific Establishment could be so wrong, for so long, so wastefully expensive in lives and effort and money, as it has been with the belief that there exists a human immunodeficiency virus, HIV, that caused and continues to cause AIDS.
Because it seems so incredible, hordes of commentators dismiss AIDS Rethinkers as denialists — in the company of other denialists, for example, those who refuse to accept that human-liberated carbon dioxide has contributed appreciably to global warming.

Since the late 19th century, “science” has been the touchstone of trustworthy knowledge. What “science” says is naturally taken by the general public, abetted by the media, as what pertinent professional organizations and acknowledged experts say. “Science” is equated with the prevailing mainstream consensus. If science is the touchstone of true knowledge, which it has seemed reasonable to believe since the end of the 19th century, HIV/AIDS theory being wrong would be an enormous, an incredibly enormous, an inexplicable aberration.

The same conundrum faces the large number of climatologists, meteorologists, atmosphere scientists, and the like who are quite sure that there is no credible evidence that the way the earth is warming has anything to do with carbon dioxide.

What: TWO incredibly enormous, inexplicable aberrations in the world of science?

Actually, there are more than two. But each one is known primarily — perhaps even only — to specialists in each given field *. The fact of the matter is that science has changed. What would have seemed an incredible aberration half a century ago has become the new normal.
That’s the message of my recent book, Dogmatism  in Science and Medicine: How Dominant Theories Monopolize Research and Stifle the Search for Truth, and earlier articles **. I found in an impressive range of specialties that minority views expressed by competent experts are not just ignored, not just argued against, they are actively suppressed by refusal of grants, refusal of resources for research, refusal of publication.
The evidence of suppression is conclusive. That does not, of course, entail that the suppressed claims are right and the mainstream wrong. It does demonstrate, however, that the traditional and conventional view of science as characterized by open argument over interpretations, and thereby reliable self-correction on the basis of evidence, does not describe accurately the contemporary scene.

But if science is now not evidence-based and self-correcting, then errors like HIV/AIDS theory are not aberrations, they are to be expected.

This is a bitter lesson for AIDS Rethinkers and other “denialists”. In order to make our case plausible to the media and the general public, we must at the same time make the case for the sea change that has overtaken “science” in the last half century or so: from generally evidence-based and thereby self-correcting to circumstances much like other social activities: heavily influenced by self-interest of the participating people and institutions.


* Suppression of science within science,, 17 December 2009

** Science in the 21st Century: Knowledge Monopolies and Research Cartels, Journal of Scientific Exploration 18 (2004) 643—660; The New World Order in Science,, 19 December 2009

9 Responses to “HIV/AIDS: Aberration or THE NEW NORMAL?”

  1. mo79uk said

    It sort of echoes what’s gone on with the BBC recently. No one believed the few who outed Jimmy Savile as a paedophile 40yrs ago, and then Newsnight follows this with an inverse error by wrongly accusing someone based on hearsay. The wanted narrative was that Savile was an angel and that an accused Tory must be guilty; it all fell apart.
    Today Rethinkers are quacks and the orthodoxy are moral, tomorrow…

  2. Michael Duggan said

    Henry, I’m on the opposite side of the fence. I think there is no validity to the non-causation argument. My belief is based on personal experience coupled with an extensive understanding of HIV science. I hold a Ph.D. in physical chemistry and am able to appreciate the subtleties of controversial debate. However I would like your response to the following scenario, that is replicated for millions of people starting therapy:
    a. Person X presents with significant opportunistic disease and tests positive for HIV antibodies.
    b. Viral load comes back with a count in the hundreds of thousands and very low immune counts.
    c. Person X starts anti-viral therapy with the latest protease inhibitor and NRTI’s that have excellent side effect profiles.
    d. Close monitoring tracks falling viral load to undetectable and increasing immune counts.
    e. Person X eventually clears the opportunistic disease and does fine.
    Can you please explain this situation under the non-causation paradigm?
    Thank you for your time.
    Michael Duggan.

    • Henry Bauer said

      Michael Duggan:
      The non-causation evidence that convinced me came from collating essentially all the HIV tests published for the USA up to the late 1990s, as set out in my book, The Origin, Persistence and Failings of HIV/AIDS Theory. Before looking at all those data, I had found plausible the doubts expressed in Root-Bernstein (Rethinking AIDS) and probably several other books, can’t recall when I read Duesberg, Shenton, and others. Bialy’s claim (in Oncogenes, Aneuploidy and AIDS) that the first tests of potential recruits from all across the USA, in mid-1980s, found female teenagers HIV+ at the same rate as male teenagers struck me as impossible, given that HIV was supposed to have entered the USA in the mid-to-late 1970s in communities of gay men. No sexually transmitted infection could spread like that within a decade, it seemed to me. So I checked Bialy’s source, and he had quoted correctly. So I thought maybe other research articles had found differently, but no… So I finished up gathering every available report of an HIV test, and the conclusion seemed obvious, that HIV+ is not infectious, not transmissible.
      I haven’t seen anything since that changes those data and that conclusion. Indeed, the original puzzle, how a sexually transmitted agent could move from gay communities to female teenagers all across the country within a decade became even more obviously impossible, given that even mainstream claims have a transmissibility of a few per thousand for unprotected acts of intercourse. Gallo himself has conceded that HIV is peculiarly difficult to transmit.
      A major difficulty in responding to your specific queries is that needed research hasn’t been done.

      a. Immune deficiency can arise from a number of known non-HIV sources.
      We don’t know what HIV antibodies might be, given that HIV has never been isolated in pure form from an authentic AIDS patient or HIV+ person. Rodney Richards, who worked at Abbott Labs on the first tests, points out that those were AIDS tests, not HIV tests: they were evolved to test poz for people ill with the opportunistic infections then said to characterize AIDS. (Note that subsequently it has turned out that the tests respond to dozens of other conditions, including TB.) The ELISA responds to some mixture of a dozen proteins. The Western Blot, not used in Britain and used with a variety of different criteria in other countries and individual institutions, takes various combinations of 2 or 3 of those proteins as positive for HIV.
      b. The inventor of PCR has stated that his technique cannot be used in the quantitative manner required for “viral load” measurements.
      c. Juliane Sacher and Claus Koehnlein, physicians in Germany, use short courses of ARVs but only when no other treatment has been able to overcome an occult undiagnosed infection or inflammation. ARVs do not specifically target HIV (which has never been isolated and characterized, as I said already).
      d. Rodriguez et al. found that viral load and CD4 counts do not necessarily track with one another nor with clinical condition.
      e. Sacher and Koehnlein use ARVs when they haven’t been able to diagnose the source of an inflammation or apparent infection, using them because they kill everything that uses RNA and DNA and makes proteins.

      No single individual case, not even a collection of them, contradicts the epidemiology, in my view. One of the most serious gaps in knowledge concerns precisely the sort of case you describe, because that gap in understanding means that persons of X’s ilk are probably not getting the best treatment, especially if the administering of ARVs continues even after any manifest OI has been cleared.
      It’s very unsatisfactory to me that I can only make negative points: HIV+ isn’t infectious, doesn’t correlate with AIDS, HIV/AIDS theory entails innumerable absurdities (e.g. breastfeeding transmits HIV, but not if breastfeeding is exclusive!). But needed research is missing with cases like Person X, to identify what non-HIV causes might be involved, and therefore how HIV+ people ought to be treated.

      I hope this is properly responsive.

      • Michael Duggan said

        Thank you for your reply. There’s a lot of info here, so please bear with me before I respond.

      • mo79uk said

        Another thing is this CDC graph from 2010 where Black American men have a disproportionate rate of infection.

        If you were to put all men in one bar and all women in another, the number of women infected altogether isn’t anywhere even half; even if for argument purposes you said 50% of the men are heterosexual or bi.

        Is there a condom use disparity? That’s possible. But I would imagine a bisexual man who doesn’t use condoms with men wouldn’t with women either.

  3. Michael Duggan said

    I’m not an expert in epidemiology – my Ph.D was in Chemistry, so unable to address the finer points of your epidemiological observations. I would say though, that the main observation over the last decade is the ever increasing life-span of people who are HIV+. This is inescabable. HIV+ people who have access to ARV’s now enjoy nearly normal life expectancies. From this observation the only reasonable deduction – in my opinion – is that the ARV’s are doing SOMETHING. Now, are they attacking the virus or treating some other disease / condition? This is the central question. I would suggest, quite strongly, that it is the virus that is being affected. This is because these drugs are specifically targeted to disrupt key enzymes – protease, reverse transcriptase, integrase – that are employed during the life cycle of HIV. Additionally, the new CCR5 blocker, Maraviroc, is designed to knock out a receptor that HIV uses to gain access T cells – a highly specific mode of action. There are some other points in your answer I would also like to address:

    You say: The inventor of PCR has stated that his technique cannot be used in the quantitative manner required for “viral load” measurements ——–> How does this tally with modern day viral load measurements that can detect down to a few viral RNA / ml?

    You say: Juliane Sacher and Claus Koehnlein, physicians in Germany, use short courses of ARVs but only when no other treatment has been able to overcome an occult undiagnosed infection or inflammation ——-> Several large trials have found significant harm from suspending ARV’s – namely, more opportunistic disease, cancers, heart disease and general morbidity / mortality.

    Again, thank you for your time.

    • Henry Bauer said

      Michael Duggan:
      Unfortunately, the devil is in the details. The epidemiology is quite clear-cut, no special technical knowledge is needed to recognize that racial and other regularities are inconsistent with an infectious agent.

      You cite a number of mainstream assertions, all of which are either disputable or plain wrong. For example, re “nearly normal life expectancies”: to prove that we would have to wait several decades, wouldn’t we?
      The decrease in mortality IMMEDIATELY upon introduction of cocktail ARVs shows that the earlier monotherapy was highly toxic, more toxic than the cocktails, not that the latter are extending life.
      The NIH Treatment Guidelines admit that serious NON-AIDS adverse events are greater in number than AIDS events among patients on ARV. Hardly lifesaving.
      The CCR5 thing concerns a small minority of cases and isn’t really pertinent to the larger picture.
      That PCR can detect tiny amounts of DNA or RNA is precisely why it can’t be used quantitatively: the amplification is so huge that any impurities or other glitches would throw things off without any way of recognizing that.

      But the main point is the details. I found it hard to believe what I was seeing as I gathered the HIV-test data, but there’s no gainsaying it. Have look at CONFESSION OF AN “AIDS DENIALIST”: How I became a crank because we’re being lied to about HIV/AIDS and some of the other articles at, especially the first three.

      Best wishes


  4. Michael Duggan said

    Again, thanks for replying. Although we hold contrary opinions, I really respect your willingness to dig into this with me. I am very interested in anomalies in science and I am sometimes on the proponent side, for example, in the psi debate, so I like to think I’m open minded in controversial debates.

    Just a few points to your last response: the normal life expectancies are derived from fairly standard statistical modelling allowing extrapolation of current death rates. These techniques are used in other areas, for example, heart disease and cancers. I see no reason why they can’t be applied to HIV mortality also.

    Agreed, AZT monotherapy in the early days was super-toxic and the Concord trial showed no benefit, and quite a lot of harm, but we know HIV+ folk off therapy live on average ten years and are clinically progressive after just a few years in a good proportion of cases. Those on triple combination are still doing well fifteen years or so after their introduction, even after starting with significant disease progression. The argument that moving from less toxic medicine is responsible for the decreased mortality I don’t think holds water.

    The CCR5 receptor is used to gain access to T cells by HIV in the majority of HIV+ folk – a minority having HIV that uses the alternative CXCR4 receptor. So I disagree about CCR5 being a minority issue. I therefore stand by my Maraviroc comment above.

    Finally regarding the PCR, how is it able to give a wide range of values from a few to millions of copies if it can’t be used quantitatively?

    Thanks for your link. I will give it a read.

    Best wishes,

    • Henry Bauer said

      Michael Duggan:
      Interest in anomalies in science is what made me change from doing chemistry to doing science studies.
      I agree that life expectancies are often ESTIMATED by statistical modeling. How reliable that is depends on how solid the various assumptions and data are.
      A central issue concerns diagnosis. HIV tests alone cannot diagnose actual HIV infection — according to a quite authoritative source, Weiss SH, Cowan EP: Chapter 8, “Laboratory detection of human retroviral
      infection”, in Wormser GP, ed. AIDS and Other Manifestations of HIV Infection, 4th ed. Academic Press, 2004—cited in those 3 articles I mentioned.
      If HIV tests are prone to false positives, it throws everything else off that’s based on accepting results of HIV tests as proving infection.
      But I’m only repeating what’s in those articles.

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s