HIV/AIDS Skepticism

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

Posts Tagged ‘Jr.’

HAART, heart disease, & lying with statistics

Posted by Henry Bauer on 2010/01/19

Brian Carter had asked: “More proof of drugs causing disease?”
in connection with the piece,
“Increased presence, severity of coronary artery plaques in HIV-infected men”
(ScienceDaily, 8 January 2010):
“The HIV-positive participants had longstanding infection, were generally healthy, and the great majority were receiving antiretroviral therapy” [emphasis added].

Seemed likely that the answer would be “Yes” to Brian’s question, so I got the original article, “Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men” (Lo et al.). I was surprised to read that duration of HIV infection was significantly associated with coronary plaque build-up “after adjustment for age, traditional risk factors, or duration of antiretroviral therapy” [emphasis added]. If HAART was causing the coronary disease, then longer HAART should correlate with more disease, surely!

Well, consider that statement carefully: It doesn’t deny that duration of antiretroviral therapy is associated with plaque build-up; it just says that HIV infection is independently associated with plaque buildup. But reading the whole article reveals that there’s actually no good evidence that plaque build-up is associated with “HIV” in absence of HAART.

Many studies have indicted HAART for increasing coronary risks, notably the protease inhibitors which disturb fat metabolism. That was reported already within a year or two of the first use of protease inhibitors, which had also been reported to produce hyperglycemia and hemolytic anemia (Massip et al.). “Use of HIV PIs is associated with atherogenic lipoprotein changes and endothelial dysfunction. Because these metabolic and vascular changes predispose to atherosclerosis, monitoring and treatment of dyslipidemia in patients taking these medications is warranted (Stein et al.).

HAART doubles the risk of coronary heart disease in young adults (Currier et al.) and “the proportion of deaths attributable to non-AIDS diseases increased and prominently included hepatic, cardiovascular, and pulmonary diseases, as well as non-AIDS malignancies. Longer time spent receiving HAART and higher CD4 cell counts at HAART initiation were associated with death from non-AIDS causes. CD4 cell count at time of death increased over time” (Palella et al.). HAART also is associated with an increased thickness of carotid-artery deposits (IMT): “Antiretroviral-treated patients had a higher median IMT than the untreated patients (0.94 vs. 0.85 mm, P = 0.006; Fig. 3). Furthermore, among all HIV-infected participants, increasing duration of HAART (rho 0.20, P < 0.001), protease inhibitor use (rho 0.19, P < 0.001), and nucleoside analogue use (rho 0.23, P < 0.001) were each associated with thicker IMT. These relationships remained significant after adjustment for traditional cardiac risk factors and the duration of HIV diagnosis (P < 0.024 for all)” (Hsue et al.).
((However, this unequivocal statement is followed by equivocations in the article’s Discussion section — “Compared to uninfected controls, carotid IMT was higher among all groups of HIV patients, irrespective of antiretroviral treatment or the level of viremia”; yet also “antiretroviral therapy and advanced immunodeficiency likely contribute independently to atherosclerosis in HIV patients”. The equivocation may be inevitable since the HIV-negative “controls” had lower coronary risk factors, so the study could not possibly identify “HIV” as the cause of more coronary disease:
“The  HIV-seropositive patients were older than the controls (48 years compared to 43 years) and more likely to have smoked in the past. The HIV-seropositive patients were also more likely to have had a prior history of coronary artery disease and a prior history of hypertension, whereas the controls had a higher LDL cholesterol [112 vs 103] and HDL cholesterol [47 vs 42.7]”. My cardiologists asserted that the risk factor is actually HDL/LDL ratio, desirably >0.3 and ideally >0.4. Here we have controls with 47/112 = 0.420, in other words no risk factor, and “HIV-positives” with 42.7/103 = 0.414, indistinguishable from controls. In other words, “HIV-positives” in this study had unquestionably higher risk factors, making any implication of “HIV” highly questionable. You can’t claim significant results if the controls aren’t proper controls, no matter how you dice and slice the numbers.))

The Treatment Guidelines issued by the National Institutes of Health surely represent an official mainstream consensus, and they are clear that HAART is associated with increased organ failure including adverse coronary events:
“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 [14-19] 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” (emphases added; p. 21, 3 November 2008).

How then could Lo et al. claim that HIV infection was significantly associated with coronary plaque build-up “after adjustment for . . . duration of antiretroviral therapy”?

In point of fact, some of the reported data do show an effect of HAART on plaque build-up — albeit there’s a certain amount of statistical legerdemain to wade through, and the need to THINK about whether the statistical calculations make sense.

The authors’ affiliations are with programs in Nutritional Metabolism, Cardiovascular Imaging, and Internal Medicine, entirely appropriate for examination of arteries and the like, but not necessarily for statistical analysis. It may be, of course, that one or more of the authors is expert in statistics, but it isn’t confidence-building to read that
“Two-tailed probability values are reported and statistical significance was assumed when P value was less than 0.05. All statistical analyses were performed using JMP (SAS Institute Inc., Cary, North Carolina, USA) and SPSS (SPSS Inc., Chicago, Illinois, USA).”
Expert statisticians tend to groan and roll their eyes heavenward when non-statisticians use such readymade statistics software packages and feed data into them without thinking knowledgeably about whether a particular mode of analysis makes sense.

Lo et al. used imaging to measure degree of atherosclerosis “in HIV-infected men”, with a sample of 78 and 32 controls of HIV-negative men matched for cardiovascular risk factors, and they found significantly more plaque in the “HIV-infected”. Then, among the HIV-infected only, they compared those with plaque (32) and those without (46) and found statistical significance at the p<0.05 level for several parameters (Age, Race, Framingham risk score, Duration since HIV diagnosis, CD4+/CD8+ T-lymphocyte ratio, Total cholesterol, Triglycerides, Cytomegalovirus titer), but not for antiretroviral treatment:

Note that ALL of the measures of HAART duration are higher in the plaque group. That these differences do not reach significance at the p<0.05 level is no evidence, however, against the previously well-established fact that antiretroviral treatment causes coronary disease. At a minimum, one would say that while the numbers do not add statistically significant evidence, they are consistent with the expectation that HAART causes coronary disease:
— For one thing, the sample sizes are not large enough to produce statistical significance in a multivariate analysis with so many variables.
— Second, comparing mean years of treatment is not the best way to look for possible causation of coronary disease. One would like to see a graph or data set showing the raw data for each individual, because one wants to test for the presence of a threshold effect or some other non-linear dose-effect or duration-effect relationship: it is perfectly feasible, perhaps even to be expected, that a certain period of years on antiretroviral treatment would produce no discernible plaque but that accumulation might progress relatively rapidly once plaque has begun to form.
— Third: One would like the data for individuals also because of certain apparent incongruities, for instance the much shorter periods on protease inhibitors than on antiretroviral treatment as a whole, since HAART is generally thought to have protease inhibitor as one of the typical components.
— Above all, though, the manner in which these numbers are presented makes it easy to overlook that the best indicator of whether HAART causes coronary disease is to compare “HIV-positive” people who have never been on HAART at all with those who have been. Here, there is no significant difference found, with p=0.16 too large. But hidden in plain view is the fact that the number of individuals NOT on HAART was only 3 in the no-plaque group and 1 in the plaque group!
NOT on HAART were 3/32  (9.4%) in the no-plaque group and 1/46 (2.2%) in the plaque group. That looks quite significant, and very different from 90.6 vs. 97.8.

“How to Lie with Statistics” by Darrell Huff (1954/1993) and “Damned lies and statistics: untangling numbers from the media, politicians, and activists” and “More damned lies and statistics: how numbers confuse public issues” by Joel Best (2001,2004) point to many other devices for presenting numbers and statistical data to produce a desired impression not necessarily warranted by the data themselves. In the present case, one can legitimately state a priori that it is unlikely to be a good test of the influence of HAART on coronary disease when the proper control group — “HIV-positive” individuals who have never experienced HAART — constitutes only 4 of the sample of 78. Further, any possible effect is hidden rather than exposed when the data are presented only as averages, which leave salient questions unanswerable. For example, the average time since HIV diagnosis is 13.5 years, yet the average duration of antiretroviral treatment is 6.2 and 7.9 years for the two groups but only 4 individuals out of 78 have never had antiretroviral treatment: How many had very short courses? Why? What were the differences in individual treatments? And so on.

Given the small sample size, one might reasonably conclude that statistical analysis could not command the power to deliver statistically significant results, and one would make do with the numbers themselves. And those numbers are perfectly consistent with all the previous reports that antiretroviral treatment increases the risk of coronary disease (and also kidney and liver disease as well as certain cancers). After all, among people never on HAART, 75% (3/4) had no sign of coronary disease and only 25% did, whereas of those who have experienced HAART, 61% showed plaque (45/74).

Above all, the data presented by Lo et al. shows a pronounced increase in cardiovascular disease with longer duration of “HIV infection” AND 74  OF  THE  78  PEOPLE  IN  THE  SAMPLE  HAD  BEEN  ON  ANTIRETROVIRAL  TREATMENT, only 4 had not, and 3 of those 4 showed no sign of cardiovascular disease. Those data are at least equally compatible with the inference that duration of HAART correlates with cardiovascular disease, and comparisons of those with and without plaques confirms that: Those with plaque had experienced antiretroviral treatment 27% longer (7.9 vs 6.2 years), particularly protease inhibitors (52% longer, 4.4 vs 2.2).

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SOURCES:
Lo et al.: Janet Lo, Suhny Abbara, Leon Shturman, Anand Soni, Jeffrey Wei, Jose A. Rocha-Filho, Khurram Nasir, and Steven K. Grinspoon, “Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men” AIDS 24 [2010] 243-53

Massip et al.: P. Massip, B. Marchou, E. Bonnet, L. Cuzin, & J. L. Montastruc, “Lypodystrophia with protease inhibitors in HIV patients”, Thérapie 52 [1997] 615

Stein et al.: James H. Stein, Melissa A. Klein, Jennifer L. Bellehumeur, Patrick E. McBride, Donald A. Wiebe, James D. Otvos, & James M. Sosman, “Use of Human Immunodeficiency Virus-1 Protease Inhibitors is associated with atherogenic lipoprotein changes and endothelial dysfunction”, Circulation 104 [2001] 257-62.

Currier et al.: Judith S. Currier, Anne Taylor, Felicity Boyd, Christopher M. Dezii, Hugh Kawabata, Beth Burtcel, Jen-Fue Maa, & Sally Hodder, “Coronary heart disease in HIV-infected individuals”, JAIDS 33 [2003] 506-12

Palella et al.: Frank J. Palella, Jr., Rose K. Baker, Anne C. Moorman, Joan S. Chmiel, Kathleen C. Wood, John T. Brooks, Scott D. Holmberg, & HIV Outpatient Study Investigators, “Mortality in the Highly Active Antiretroviral Therapy era — Changing causes of death and disease in the HIV Outpatient Study” JAIDS 43 [2006] 27-34

Hsue et al.: Priscilla Y. Hsue, Peter W. Hunt, Amanda Schnell, S. Craig Kalapus, Rebecca Hoh, Peter Ganz, Jeffrey N. Martin & Steven G. Deeks, “Role of viral replication, antiretroviral therapy, and immunodeficiency in HIV-associated atherosclerosis”, AIDS 23 [2009] 1059-67

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Believing and disbelieving

Posted by Henry Bauer on 2009/07/03

(This is a long post. HERE is a pdf for those who prefer to read it that way).

“How could anyone believe that?” is a natural question whenever someone believes what is contrary to the conventional wisdom, say, that HIV doesn’t cause AIDS, or that Loch Ness monsters are real animals.

Since the role of unorthodox views in and out of science has been the focus of my academic interests for several decades, I had to think about that question in a variety of contexts. My conclusion long ago was that this is the wrong question, the very opposite of the right question, which is,

“How does anyone ever come to believe differently than others do?” (1)

********************

It’s a widespread illusion that we believe things because they’re true. It’s an illusion that we all tend to harbor about ourselves. Of course I believe what’s true! My beliefs aren’t wrong! It’s the others who are wrong.

However, we don’t acquire beliefs because they’re true, we acquire them through being taught that they’re true. For the first half-a-dozen or a dozen years of our lives, before we have begun to learn how to think truly for ourselves, as babies and children we almost always believe what parents and teachers tell us. Surely that has helped the species to survive. But no matter what the reason might be, there’s ample empirical evidence for it. For instance, many people during their whole lifetime stick to the religion that they imbibed almost with mother’s milk; those who reject that religion do so at earliest in adolescence.

That habit of believing parents and teachers tends to become ingrained. Society’s “experts”  — scientists and doctors, surrogate parents and teachers — tend to be believed as a matter of habit.

So how do some people ever come to believe other than what they’ve been taught and what the experts say?

**********************

I was prompted to this train of thought by receiving yet again some comments intended for this blog and which were directed at minor details, from people whom I had asked, long ago, to cut through this underbrush and address the chief point at issue: “What is the proof that HIV causes AIDS?”

Whenever I’ve asked this of commentators like Fulano-etc.-de-Tal, or Chris Noble, or Snout, or others who want to argue incessantly about ancillary details, the exchange has come to an end. They’ve simply never addressed that central issue.

And it’s not only these camp followers. The same holds for the actual HIV/AIDS gurus, the Montagniers and Gallos and Faucis. Fauci threatens journalists who don’t toe the orthodox line. Gallo hangs up on Gary Null when asked for citations to the work that made him famous.

Why can’t these people cite the work on which their belief is supposedly based?

Finally it hit me: Because their belief wasn’t formed that way. They didn’t come to believe because of the evidence.
The Faucis and Gallos came to believe because they wanted to, because a virus-caused AIDS would be in their professional bailiwick, and they were more than happy to take an imperfect correlation as proof of causation.
The camp followers came to believe simply because they were happy to believe what the experts say and what “everyone else” believes. Who are they to question the authority of scientific experts and scientific institutions?

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To question “what everyone knows”, there has to be some decisive incentive or some serendipitous conjunction. I’ll illustrate that by describing how I came to believe some things that “everyone else” believes and some things that “everyone else” does not believe.

The first unorthodox opinion I acquired was that Loch Ness monsters are probably real living animals of some unidentified species. How did I come to that conclusion?
Serendipity set the stage. Reading has been my lifelong pleasure. I used to browse in the local library among books that had just been returned and not yet reshelved, assuming that these would be the most interesting ones. Around 1961, I picked from that pile a book titled Loch Ness Monster, by Tim Dinsdale. I recall my mental sneer, for I knew like everyone else that this was a mythical creature and a tangible tourist attraction invented by those canny Scots. But I thumbed the pages, and saw a set of glossy photos: claimed stills from a film! If these were genuine . . . . So I borrowed the book. Having read it, I couldn’t make up my mind. The author seemed genuine, but also very naïve. Yet his film had been developed by Kodak and pronounced genuine. Could it be that Nessies are real?
I was unable to find a satisfactory discussion in the scientific literature. So I read whatever other books and articles I could find about it. I also became a member of the Loch Ness Investigation, a group that was exploring at Loch Ness during the summers, and I followed their work via their newsletters — I couldn’t participate personally since I then lived in Australia.
A dozen years later, on sabbatical leave in England, I took a vacation trip to Loch Ness. More serendipity: there I encountered Dinsdale. Later I arranged lecture tours for him in the USA (where I had migrated in 1965). Coming to know Dinsdale, coming to trust his integrity, seeing a 35mm copy of his film umpteen times during his talks, brought conviction.
It had taken me 12-15 years of looking at all the available evidence before I felt convinced.

The unorthodox view that underwrites this blog is that HIV doesn’t cause AIDS. How did I come by that belief in something that “everyone else” does not believe?
More serendipity. Having concluded in the early 1970s that Nessies were probably real, I became curious why there hadn’t been proper scientific investigations despite the huge amount of publicity over several decades. That led eventually to my change of academic field from chemistry to science studies, with special interest in heterodoxies. So I was always on the lookout for scientific anomalies and heresies to study. In the mid-1990s, I came across the book by Ellison and Duesberg, Why We Will Never Win the War on AIDS (interesting info about this here ; other Ellison-Duesberg articles here).
Just as with Dinsdale’s book, I couldn’t make up my mind. The arguments seemed sound, but I didn’t feel competent to judge the technicalities. So, again, I looked for other HIV/AIDS-dissenting books, and wrote reviews of a number of them. Around 2005, that led me to read Harvey Bialy’s scientific autobiography of Duesberg. For months thereafter, I periodically reminded myself that I wanted to check a citation Bialy had given, for an assertion that obviously couldn’t be true, namely, that positive HIV-tests in the mid-1980s among teenage potential military recruits from all across the United States had come equally among the girls as among the boys. The consequences of checking that reference are described in The Origin, Persistence and Failings of HIV/AIDS Theory.
As with Nessie, it had taken me more than ten years of looking into the available evidence to become convinced of the correctness of something that “everyone else” does not believe.

So am I saying that I always sift evidence for a decade before making up my mind?
Of course not. I did that only on matters that were outside my professional expertise.

Studying chemistry, I didn’t question what the instructors and the textbooks had to say. I surely asked for explanations on some points, and might well have raised quibbles on details, but I didn’t question the periodic table or the theory of chemical bonding or the laws of thermodynamics or any other basic tenet.

That, I suggest, is quite typical. Those of us who go into research in a science don’t begin by questioning our field’s basic tenets. Furthermore, most of us never have occasion to question those tenets later on. Most scientific research is, in Kuhn’s words (2), puzzle-solving. In every field there are all sorts of little problems to be solved; not little in the sense of easy, but in the sense of not impinging on any basic theoretical issues. One can spend many lifetimes in chemical research without ever questioning the Second Law of thermodynamics, say, or quantum-mechanical calculations of electron energies, and so on and so forth.

So: Immunologists and virologists and pharmacologists and others who came to do research on HIV/AIDS from the mid-1980s onwards have been engaged in trying to solve all sorts of puzzles. They’ve had no reason to question the accepted view that HIV causes AIDS, because their work doesn’t raise that question in any obvious way; they’re working on very specialized, very detailed matters — designing new antiretroviral drugs, say; or trying to make sense of the infinite variety of “HIV” strains and permutations and recombinations; or looking for new strategies that might lead to a useful vaccine; and so on and so forth. Many tens of thousands of published articles illustrate that there are no end of mysterious puzzles about “HIV/AIDS” waiting to be solved.

The various people who became activist camp followers, like the non-scientist vigilantes among the AIDStruth gang, didn’t begin by trying to convince themselves, by looking into the primary evidence, that the mainstream view is correct: they simply believed it, jumped on the very visible bandwagon, took for granted that the conventional view promulgated by official scientific institutions is true.

It is perfectly natural, in other words, for scientists and non-scientists to believe without question that HIV causes AIDS even though they have never seen or looked for the proof.

What is not natural is to question that, and the relatively small number of individuals who became HIV/AIDS dissidents, AIDS Rethinkers, HIV Skeptics, did so because of idiosyncratic and specific reasons. Women like Christine Maggiore, Noreen Martin, Maria Papagiannidou, Karri Stokely, and others had the strongest personal reasons to wonder about what they were being told: since they had not put themselves at risk in the way “HIV” is supposedly acquired, and since they were finding the “side” effects of antiretroviral drugs intolerable, the incentive was strong to think for themselves and look at the evidence for themselves.
Many gay men have had similar reason to question the mainstream view, and some unknown but undoubtedly large number of gay men are living in a perpetual mental and emotional turmoil: on one hand much empirical evidence of what the antiretroviral drugs have done to their friends, on the other hand their own doctors expressing with apparent confidence the mainstream view. So only a visible minority of gay men have yet recognized the failings of HIV/AIDS theory.
One of the first to do so, John Lauritsen, was brought to question the mainstream view for the idiosyncratic personal reason that, as a survey research analyst, he could see that the CDC’s classification scheme was invalid.
Among scientists, Peter Duesberg recognized some of the errors of HIV/AIDS theory because he understood so much about retroviruses and because he had not himself been caught up in the feverish chase for an infectious cause of AIDS. Robert Root-Bernstein, too, with expertise in immunology , could recognize clearly from outside the HIV/AIDS-research establishment the fallacy of taking immunedeficiency as some new phenomenon. Other biologists, too, who were not involved in HIV/AIDS work, could see things wrong with HIV/AIDS theory: Charles A. Thomas, Jr., Harvey Bialy, Walter Gilbert, Kary Mullis, Harry Rubin, Gordon Stewart, Richard Strohman, and many others who have put their names to the letter asking for a reconsideration.

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To summarize:

Mainstream researchers rarely if ever question the basis for the contemporary beliefs in their field. It’s not unique to HIV/AIDS. HIV/AIDS researchers and camp followers never cite the publications that are supposed to prove that HIV causes AIDS for the reason that they never looked for such proof, they simply took it for granted on the say-so of the press-conference announcement and subsequent “mainstream consensus”.

The people who did look for such proof, and realized that it doesn’t exist, were:
—  journalists covering “HIV/AIDS” stories (among those who wrote books about it are Jad Adams, Elinor Burkett, John Crewdson, Celia Farber, Neville Hodgkinson, Evan Lambrou, Michael Leitner, Joan Shenton);
—  directly affected, said-to-be-HIV-positive people, largely gay men and also women like those mentioned above;
—  individuals for a variety of individual reasons, as illustrated above for John Lauritsen and myself;
—  scientists in closely related fields who were not working directly on HIV/AIDS.

That last point is pertinent to the refrain from defenders of HIV/AIDS orthodoxy that highly qualified scientists like Duesberg or Mullis are not equipped to comment because they have never themselves done any research on HIV or AIDS. But that’s precisely why they were able to see that this HIV/AIDS Emperor has no clothes — scientists working directly on the many puzzles generated by this wrong theory have no incentive, no inclination, no reason to question the hypothesis; indeed, the psychological mechanism of cognitive dissonance makes it highly unlikely that scientists with careers vested in HIV/AIDS orthodoxy will be able to recognize the evidence against their belief.
More generally, this is the reason why the history of science contains so many cases of breakthroughs being made by outsiders to a particular specialty: coming to it afresh, they are not blinded by the insider dogmas.

So there is nothing unique about the fact that the failings of HIV/AIDS theory have been discerned by outsiders and not by insiders, and that the insiders are not even familiar with the supposed proofs underlying their belief. Nor is it unique that the dogma has many camp followers who never bothered to look for the supposed proofs of the mainstream belief. What is unique to HIV/AIDS theory is the enormous damage it has caused, by making ill or actually killing hundreds of thousands (at least). The annals of modern medicine have no precedent for this, which is another reason why thoughtless supporters of HIV/AIDS orthodoxy may feel comfortable with it despite never having sought evidence for it.

So here’s the question to put to everyone who insists that HIV causes AIDS:

HOW  DID  YOU  COME  TO  BELIEVE  THAT?
WHAT  CONVINCED  YOU?

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Cited:
(1) Henry H. Bauer, Beyond Velikovsky: The History of a Public Controversy, University of Illinois Press, 1984; chapter 11, “Motives for believing”.
(2) Thomas S. Kuhn, The Structure of Scientific Revolutions, University of Chicago Press, 1970 (2nd ed., enlarged; 1st ed. 1962)

Posted in experts, HIV does not cause AIDS, HIV skepticism, prejudice | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | 10 Comments »

 
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