HIV/AIDS Skepticism

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

Archive for May, 2008


Posted by Henry Bauer on 2008/05/19

Proponents of HIV/AIDS theory are on the classical horns of a syllogistic dilemma:
1. Racial disparities as to testing “HIV-positive” are pervasive, constant, and universally acknowledged. It is undeniable that people of recent African ancestry test “HIV-positive” many times more often than others, in all social groups and economic circumstances. Testing “HIV-positive” goes with recent African ancestry as inevitably as does dark-hued skin.
2. Under HIV/AIDS theory, the tendency to become “HIV-positive” is ascribed primarily to types of behavior that are widely disdained.
3. Thereby such disdained behavior is linked inevitably to race.

That conclusion is contrary to what’s nowadays well known about the independence of behavior and genotype, and it is blatantly racist. Point 3., what the syllogism presents as demonstrated, being ignorant as well as racist (but then racism is in any case a sub-category of ignorance) means that at least one of points 1. and 2. is wrong. Which one?

The evidence for 1. is, as already stated, undisputed. Many illustrative sources are cited in The Origin, Persistence and Failings of HIV/AIDS Theory. Others have been added in many earlier posts (HIV AND SEXUALLY TRANSMITTED DISEASE: IT JUST ISN’T SO, 28 November; “HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008; REGULAR AS CLOCKWORK: HIV, THE TRULY UNIQUE “INFECTION”, 1 April 2008; HIV: THE VIRUS THAT DISCRIMINATES BY RACE, 11 April 2008; HIV: A RACE-DISCRIMINATING SEXUALLY TRANSMITTED VIRUS!, 16 April 2008; DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008 ). Perhaps the most striking demonstrations that it is biological, physical, race that determines rates of testing “HIV-positive” are the difference between Hispanics on the East and West coasts in the United States, and that in South Africa the “coloreds”, of mixed racial ancestry, test positive at rates intermediate between those seen with blacks and with whites.

Since point 1. is correct, and point 3. is wrong, therefore point 2. must also be wrong.

Indeed, the evidence against point 2. is just as solid as the evidence for point 1.; for sources and discussion, see WHAT “HIV” IS NOT: IT’S NOT SEXUALLY TRANSMITTED, 6 January 2008 and Chapter 4 in The Origin, Persistence and Failings of HIV/AIDS Theory.

What’s so difficult to accept, to comprehend, to explain, is that the conventional wisdom has ignored this evidence for so long and with such passionate determination.

In order not to admit that point 2. — that “HIV” is sexually transmitted — is in error , it is necessary to recast point 3. in a manner that masks its erroneous and racist nature. How to do this?

“The promiscuity, blind sexual trust and intravenous drug use that gave life to this incurable disease is just as prevalent today as when former NBA great Magic Johnson gave HIV/AIDS a recognizable face. Black people in Mississippi make up 70 percent of the new HIV/AIDS cases; black women make up 49 percent. No major study exists to tell us why, so we’re left with theories that have no scientific foundation” (Ronnie Agnew, “HIV’s new target: Black women”, Clarion-Ledger [Jackson, MS], 23 April 2006).

Political correctness offers a working model for obfuscating the matter: Accept that undesirable behavior is linked to race, but assert that this is only because race has meant discrimination and its after-effects of deprivation, poverty, lack of health care, etc. In other words, “their” behavior is admittedly despicable, but it’s not really their fault.

Thus, as Potterat pointed out recently, there has been “evidence and speculation that epidemic trajectories are shaped by demographic, social, economic and network configurations” (“Blind spots in the epidemiology of HIV in black Americans”, Int J STD & AIDS 19 [2008] 1-3).

The currently fashionable parlance among HIV/AIDS experts is “multiple concurrent relationships”. That abstract mouthful fails to reveal the magnitude of sexual activity required to explain the spread of HIV: 20-40% of the population must be having sex with several people during the same short period of time and all the people involved must be changing partners every weeks (B***S*** about HIV from ACADEME via THE PRESS, 4 March 2008). A colloquial description of such behavior allegedly found among Africans and African Americans might be, “Those macacas screw around in ways that us civilized folks don’t”.

(For the expression “macaca” I am indebted to Republican Senator and former Governor of Virginia, George Allen, whose use of it on a public occasion is widely thought to have spelled the demise of his campaign for the presidential nomination of his party.)


In any case, no one attempts to deny the statistical facts. Under HIV/AIDS theory, those facts must be interpreted in racist fashion, relying on racist stereotypes as to sexual behavior. The mainstream attempt to hide that inescapable fact, to obfuscate it, harnesses nice-sounding, politically correct, words like “cultural differences” and references to “minorities” in relation to “poverty”, “discrimination”, lack of access to health case, and the like. What that amounts to is admitting that “they”, the macacas, do behave that way, but it isn’t really their individual or collective fault. Here are some actual examples of this rhetoric:

“The marked racial and ethnic differences in HIV prevalence, even among persons treated in the same clinic, suggests that both behavioral norms and complex social mixing patterns within racial and ethnic groups are important determinants of HIV transmission risk” (emphasis added; Centers for Disease Control and Prevention, HIV/AIDS surveillance report for 1992, p. 37).
Translating from jargon: “behavioral norms” = regarded as acceptable behavior; “complex social mixing patterns” = those who behave improperly are not sexually segregated from others “within racial and ethnic groups”.

Nor has the Centers for Disease Control and Prevention changed its belief since then, as they informed me in 2005: “The ‘characteristic differentiation by race’ that you note is compatible with a behavioral explanation” (emphasis in original, Shari Steinberg [Divisions of HIV/AIDS Prevention, CDC], letter to Henry Bauer, 19 May 2005).

“The phenomenon of men on the down low has gained much attention in recent years; however, there are no data to confirm or refute publicized accounts of HIV risk behavior associated with these men. What is clear is that women, men, and children of minority races and ethnicities are disproportionately affected by HIV and AIDS … .
What steps is CDC taking to address the down low?
CDC and its many research partners have several projects in the field that are exploring the HIV-related sexual risks of men, including men who use the term down low to refer to themselves. The results of these studies will be published in medical journals and circulated through press releases in the next few years as each study is concluded and the data analyzed. CDC has also funded several projects that provide HIV education, counseling, and testing in minority racial and ethnic communities. CDC’s research and on-the-ground HIV prevention efforts will continue as more information about the demographics and HIV risk behaviors of men who do and men who do not identify with the down low becomes available” (emphasis added; unchanged since at least March 2006, accessed 11 May 2008).

Note the weasel-word “minority” used here, as so often in similar contexts. It doesn’t mean minority, it’s a euphemism for “black”. Asian-Americans are less affected by “HIV” than are whites, and at 4.5% of the population they surely qualify as a “minority”, certainly by comparison with about 13% African Americans. Perhaps the smallest recognized minority group in the United States is comprised of Native Americans, who are affected by “HIV” almost as little as are white Americans. The persistent usage of “minority” is intended to mask the fact that it is blacks who are so disproportionately affected, and simultaneously to suggest — in condescending and demeaning terms — that it isn’t their fault, because it’s so well known that “minorities” are devastatingly discriminated against.

It’s hard to believe that this usage of “minority” is other than deliberate. Its use implies quite clearly that the user accepts that “black” is the determining factor. The only way to explain that under HIV/AIDS theory is by differences in sexual behavior. But one mustn’t say that, even though it is evidently believed by those who resort to these euphemisms. In other words, these statements are made by people who harbor stereotypically racist beliefs — albeit they would likely be horrified if made aware of that subconscious or suppressed belief.

Posted in HIV and race, HIV risk groups, HIV tests, HIV transmission, HIV/AIDS numbers, sexual transmission | Tagged: , , , | Leave a Comment »


Posted by Henry Bauer on 2008/05/16

Linus Pauling created an astonishing number of significant advances in the chemical sciences, including the theory of chemical bonding and the physicochemical basis of biological activity, and he was the first to discover the molecular basis of a disease, the misshapen structure of hemoglobin in sickle-cell anemia.

Pauling’s political activism against the testing of nuclear weapons in the atmosphere made him something of a pariah in political circles, and his insistence on the dangers of the radioactive fallout produced in the tests was pooh-poohed by the expert white-coated gurus of the establishment. For a long time now, of course, his view on that has been the mainstream consensus, though I am not aware that there’s ever been a public acknowledgment that Pauling had been right and that the Government and its experts had been wrong.

For his chemical work, Pauling received a Nobel Prize. For his political activism, another Nobel Prize, for Peace. But when he began to stump for the desirability of large doses of vitamin C in particular, as well as the benefits of other supplements, he was labeled a crackpot who had lapsed into senility. Yet his argument for such “orthomolecular” practice was eminently reasonable: he pointed out that the “minimum daily requirements” established for vitamins and minerals were based only on clinical knowledge of the minimum amounts needed to avoid illness; it seems very likely that the optimum amounts for healthy functioning would be greater than those minimum amounts. As to vitamin C, he pointed out that our vegetarian primate cousins get far more of it from their diet than we do.

In dribs and drabs, here and there, consensus medicine has been catching up to Pauling; for instance, we are informed that senior citizens should take supplements of vitamin D, and ophthalmologists advise vitamin E, selenium, and zinc to stave off macular degeneration. At the same time, determined “crank busters” and representatives of consensus medicine continue to castigate anyone who recommends a mineral, vitamin, or other supplement that has not already been approved by the bureaucracies.

One result is that periodically a “breakthrough” is announced that comes as no news at all to people who know about these historical facts. For example, two recent articles report the discovery that for Africans seriously ill from TB, and sometimes even “HIV-positive”, “micronutrient supplements appeared to decrease the risk of early tuberculosis recurrences among HIV-positive patients”, and they “significantly decreased… incidence of peripheral neuropathy, regardless of HIV status.”

(Peripheral neuropathy is described as “a condition that can be caused by both HIV infection and key medication used to treat tuberculosis”. The second statement is correct, but the first is not; it is antiretroviral drugs, not “HIV infection”, that causes peripheral neuropathy. This is the same sleight-of-mouth as when there’s talk of “HIV-associated lipodystrophy”—the lipodystrophy comes from the drugs, chiefly the protease inhibitors. Lipodystrophy was not a widespread condition among AIDS victims or “HIV-positive” people before the advent of HAART.)

“Micronutrients”, then, offer benefits to Africans suffering from TB and also “HIV-positive”. Still, castigation and calumny are heaped upon Dr. Matthias Rath for his research on the role of nutrition in various illnesses, including HIV/AIDS, and his advocacy of a variety of supplements. Rath had worked with Linus Pauling and had been Director of Cardiovascular Research at the Linus Pauling Institute in Palo Alto (CA). Rath is now vilified just as Pauling was; and just as with Pauling, some of Rath’s insights are likely to be accepted belatedly by consensus medicine. And just as with Pauling, Rath is unlikely to be then given his due credit. From the Pooh-Bah point of view, the misunderstanding needs to be preserved, that the mainstream consensus in medicine and in science is always right.

Posted in Alternative AIDS treatments, experts, HIV skepticism | Tagged: , , , , , | 5 Comments »

SEX, RACE, and “HIV”

Posted by Henry Bauer on 2008/05/14

Proponents of HIV/AIDS theory claim that purported epidemics of “HIV” reflect primarily sexual behavior (except in Eastern Europe, where 85% of it is ascribed to drug abuse — see HIV/AIDS ILLUSTRATES COGNITIVE DISSONANCE, 29 April 2008 — implying a truly inconceivably prodigious sharing of infected needles).

Everywhere in the world, people test “HIV-positive” according to their race. People of African ancestry test positive far more often than others. Asians always test positive least frequently. Caucasians, Native Americans, and non-black Hispanics are in between, but much closer to Asians than to Africans.

Therefore, the orthodox view as to HIV/AIDS postulates, implicitly but inescapably, that members of different racial groups display characteristically different, race-determined sexual behavior.

So egregious is this assertion that I would have thought it sufficient, in and of itself, to disabuse anyone and everyone of the notion that “HIV” could possibly be a sexually transmitted agent. Consider and compare the furor over an oft-claimed association of IQ and race. The claim led to excruciatingly detailed dissection of what IQ tests actually measure. Even those who claim that there is an association between race and IQ also acknowledge that it is only probabilistic, not fully determinant (typically, heredity is said to be responsible for only about half of the variations in IQ). If there is indeed such an association of race and IQ, one could at least speculate about a possible physical or physiological and therefore genetic basis for it, by analogy with the folklore — favored by devotees of table tennis — that Asians tend to have faster reflexes, and that faster reflexes make for better IQ-test scores. But in the purported association of testing “HIV-positive” and race, no careful dissection of what the “HIV” tests measure has been carried through (except, of course, by HIV/AIDS rethinkers). In particular, it has never been shown that testing “HIV-positive” denotes active infection, as the orthodoxy maintains. Indeed, there’s a substantial prize ($25,000, plus a matching amount to charity) awaiting anyone who can produce a publication proving that “HIV-positive” means active infection (, May 2007 under “News and Updates”). There is an even larger prize for proof of the very existence of “HIV”: the Michael Verney-Elliott Memorial Prize of £50,000 .

As to whether sexual behavior might be determined definitively by race-associated genetics, I am not aware that anyone has been so foolish as to suggest it explicitly. Behavior is determined by culture, learning, environment, within very wide limits set by human genetics. Sexual mores and sexual practices have changed dramatically over short periods of time in several individual cultures without any change in racial composition of the populations expressing those cultures. Monogamy and polygamy have been practiced at times within cultures whose members belong to different racial groups. The notion that any form of behavior is directly determined by race has been thoroughly undermined by understanding and knowledge accumulated in anthropology, sociology, developmental biology, psychology, and so on. Nevertheless, the orthodox view of HIV/AIDS implies such an association, for the racial disparities in testing “HIV-positive” are at least as firmly reproducible as anything else about HIV/AIDS.

Not only does HIV/AIDS theory incorporate by clear implication the extraordinary claim that sexual behavior is characteristic of race, the sexual behavior it ascribes to Africans is implausible in the extreme.

Since the average probability of apparently transmitting “HIV” is about 1 per 1000, to produce an epidemic would seem to call for extensive and incessant orgies, a high rate of intercourse among continually changing sexual partners. In order to save the hypothesis of sexual transmission in the face of this implausible scenario, the speculation was ventured long ago (Anderson & May, Nature 333 [1988] 514-9) — and has since become generally accepted without proof — that when a person is first infected, there might ensue a short period of weeks, at most months, during which the infectivity must be much higher than 1 per 1000.

However, the highest estimates for this putative initial infectivity allowed by actual data on apparent transmission are only 1/50 to 1/250 (Cohen & Pilcher, Journal of Infectious Diseases 191 [2005] 1391-3). Such a rate still requires prodigious feats of sexual promiscuity to explain the levels of “HIV infection” reported for sub-Saharan Africa, which are greater than 20%, remember, sometimes even above 35%, in Botswana, Lesotho, Namibia, South Africa, Swaziland, and Zimbabwe (21 April 2008, DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”).

James Chin, former epidemiologist for California and later for the World Health Organization, has carried out the requisite calculations (The AIDS Pandemic: The collision of epidemiology with political correctness, Radcliffe 2007): “epidemic HIV transmission requires a very high level of HIV risk behaviors” (pp. 44, 45). To achieve an epidemic spread over a period of “many years”, 20-40% of adults must have “multiple concurrent relationships” — several sexual partners at the same time, changing to new partners weekly or monthly, totaling to tens of different partners over the course of each year (p. 64, Table 5.1). (Chin does not seem specifically to consider the postulated short periods of higher infectivity. However, doing so would then require even more rapid change of partners to produce an epidemic since the window of opportunity for transmission is so brief.)

That, then — according to the official view — is what must have been going on in “sub-Saharan Africa” for many years. Also on the official view, as one travels from south to north one would observe the level of sexual activity steadily decreasing, until in North Africa promiscuity is at quite a low level, comparable to that in the civilized regions of the developed world; see the maps in DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008.

These staggering estimates, 20-40% of adults in multiple concurrent partner-changing relationships, are not usually cited, perhaps because they are so truly not worthy of belief. Instead, what HIV/AIDS theory implies — actually demands — is masked by abstract jargon not translated into concrete quantitative scenarios: it’s just said typically that the HIV/AIDS epidemic in sub-Saharan Africa results primarily from multiple concurrent relationships among heterosexuals in overlapping networks of partners. That sort of longwinded discourse in sociological jargon allows lay people’s eyes to glaze over and to defer to the experts who surely must know what they’re talking about. But the concrete fact behind that abstract jargon remains what Chin calculated: between 20% and 40% of adults having sex with several partners during the same period of time, all of them changing those partners every few weeks. It boggles the mind. Try to imagine that in your neighborhood: between 20% and 40% of men would have several mistresses, changing them every few weeks or months for new ones, and the women would be no less promiscuous. Just about everyone would have to be doing it, and certainly everyone would know about it.

Moreover, that degree of sexual activity would surely be causing to spread also the commonly known sexually transmitted infections (STIs or STDs) — gonorrhea, syphilis, chlamydia, etc. Those are transmitted with probabilities that are far greater, ten times higher or more, than that of 1 per 50, the highest short-period rate postulated for HIV. Wherever “HIV” is spreading, therefore, the population should have been absolutely swamped by the common STDs. They are not. This in itself offers direct observational proof that HIV is not sexually transmitted, proof available to anyone who looks even cursorily at the evidence.


Now that HIV/AIDS in the United States is acknowledged to have become a disease of black communities, similar feats of sexual activity as postulated for Africa have to be imagined there as well. A high rate of “multiple concurrent relationships” has indeed been offered explicitly as partial explanation for the purported epidemics now said to be endangering, in particular, young black women, notably in the Southeast and in Washington city, DC; see, among many available examples, Kulik et al., American Journal of Public Health 85 (1995) 1119-22; Hammett et al., Sexually Transmitted Diseases 33 (2006, July suppl.) 817-22; Adimora et al., Annals of Epidemiology 14 (#3, 2004) 155-60.


The racial disparities in testing “HIV-positive” are clearly, obviously, inescapably incompatible with HIV/AIDS theory. If “HIV” were sexually transmitted, then the racial disparities in “HIV-positive” would mean that human racial groups differ characteristically and drastically in their sexual behavior and mores. Furthermore, if “HIV” were sexually transmitted, then wherever there is “HIV”, there would be vastly greater incidence of gonorrhea, syphilis, chlamydia, herpes, etc.

The notion that “HIV” is a sexually transmitted infection is simply unsustainable in light of the actual data.

Posted in HIV absurdities, HIV and race, HIV risk groups, HIV transmission, HIV/AIDS numbers, sexual transmission | Tagged: , , , , , , , , , , | Leave a Comment »


Posted by Henry Bauer on 2008/05/12

How to entice into “rethinking AIDS”, into questioning the conventional wisdom, people who have been thoroughly brainwashed by the constant repetition of “HIV, the virus that causes AIDS”?

A large part of the problem is that the rethinkers’ case is not readily made in a convincing way via self-evident sound-bites. “The ‘HIV’ tests don’t detect a virus”, or “ ‘HIV’ tests have never been proven to be specific for ‘HIV’”, while perfectly true, are based on evidence that is too technical for most people to feel comfortable with; to appreciate the strength of the case against HIV/AIDS theory, to appreciate that those mainstream-contradicting sound-bites are really true, requires prolonged immersion in much data. Even the most concise as well as documented overview, say, Christine Maggiore’s excellent What If Everything You Thought You Knew About AIDS Was Wrong?, or Rebecca Culshaw’s similarly concise yet also comprehensive Science Sold Out: Does HIV Really Cause AIDS?, are hardly bed-time reading. A promising alternative approach is through “fiction”.

There’s a long and respectable history of literary fiction that aims to acquaint readers with important facts. (Most good literature teaches at least indirectly about people and about human life, of course, but I’m now referring to deliberately didactic treatments of specific issues.) Sinclair Lewis in Martin Arrowsmith conveyed important truths about medical practice and medical research and commercial conflicts of interest. Upton Sinclair revealed through novels some ugly truths about the meat-packing industry (The Jungle), the oil industry (Oil), and others, and his Lanny Budd series can serve as a descriptive political history of the era of Nazism, the Second World War, and its aftermath. Most recently, Michael Crichton exposed the lacunae and fault lines in the current obsession with man-caused global warming in State of Fear.

HIV/AIDS seems a natural candidate for this sort of treatment, and Stephen Davis has put his hand, head, and heart into the endeavor. His first novel, Wrongful Death: The AIDS Trial, was published in 2006; the second, Are You Positive?, appeared this year.

Both books feature legal trials, and are thereby consistent with my growing suspicion that HIV/AIDS theory will only be overturned when the mainstream is forced, in a court of law, to reveal the extent to which the theory is like an Emperor wearing no clothes at all.

Wrongful Death tells the story of a class-action suit brought by relatives of those who died needlessly because “HIV-positive” people were treated with AZT. The novel was exceptionally timely, given that the Centers for Disease Control and Prevention was just then recommending that “HIV”-testing should become routine. If that were to happen, then a few perfectly healthy people in every thousand would be misguidedly told that they harbor a deadly virus and should begin taking drugs whose “side” effects make the rate of “adherence to treatment” quite low and which ultimately reward compliant adherence with serious illness and often death.

Davis follows, for legal reasons, the convention of claiming fictional character for the protagonists (except for a few well-known public figures), but readers at all familiar with HIV/AIDS matters will recognize many of the characters, most of whose names are faithful to the initials of their real-life models. The story is told in quite a straightforward manner, an appropriate vehicle for acquainting readers with the facts in a steady succession of digestible pieces. Though the story is straightforwardly told, there are also a couple of ingenious twists in the plot.

Are You Positive? features a trial that has, unfortunately, some real-life precedents: an HIV-positive man on trial for transmitting the virus to a sexual partner. As in the earlier book, the real-life models of some protagonists are recognizable, including by their initials. The evidence is unfolded at digestible pace: the lack of validity of “HIV” tests, the racial bias of the tests, the particular likelihood that TB patients and pregnant women will test “HIV-positive”. The recommendation that everyone be tested is mentioned, and the gruesome story of the orphans used as guinea pigs in clinical trials. The Padian study revealing lack of sexual transmission is dissected expertly. Gallo’s scientific failings are described accurately, as well as his self-incriminating testimony in the Parenzee trial in Adelaide (Australia). The role of conflicts of interest in the HIV/AIDS industry is brought out. An Appendix has a recommended “Informed Consent” form that people should require their doctors to sign if they are being asked to take an HIV test.

The story is told very accurately indeed in this novel. Because I already knew that every detail is correct, I found it emotionally difficult reading–I know of a dozen people languishing in jail for the crime of making love while testing “positive” for a supposedly active infection that the tests cannot actually establish, and there are surely many more in jail of whom I am not aware. HIV/AIDS-naïve readers, however, may not experience that emotional burden as they are led slowly to doubt what the conventional wisdom insists on.

My respect for these books and their author was only increased when, toward the end, I found cited one of my favorite epigrams, one I had used myself for years as the motto of a newsletter I once edited:

All that is necessary for the triumph of evil is for good men to do nothing

Both these books are paperbacks published via automated “on demand” printing. Their material quality is comparable with such productions from large publishers, but in their lack of typographical errors they are far superior to most contemporary works, including in hard covers from long-established and respected presses.

Rethinkers ought to consider giving these books to their friends and acquaintances who scoff at the possibility that the mainstream could be wrong about HIV/AIDS. Leading HIV/AIDS-naïve people through salient details of the evidence in measured and linear succession is likely to make it easier for them to begin to shake off unthinking acceptance of the conventional wisdom than trying to argue all the scientific issues in concentrated form. Wrongful Death cites hundreds of supporting published sources; Are You Positive? relegates them to the website. In both cases, you can assure those to whom you give these books that the cited evidence is solidly supported in the mainstream literature and that the cited sources represent fairly the totality of what has been published and what is known.

Posted in antiretroviral drugs, HIV does not cause AIDS, HIV tests, Legal aspects, sexual transmission | Tagged: , , , , , , , , , , , | 2 Comments »


Posted by Henry Bauer on 2008/05/09

No sooner had I remarked on cognitive dissonance (HIV/AIDS ILLUSTRATES COGNITIVE DISSONANCE, 29 April 2008 ) than a truly hair-raising instance of it turns up: the increasing rate of deaths caused by antiretroviral drugs is said to require clinical trials in which these drugs would be tried out on even healthier people.


Most “AIDS” deaths now are from liver failure, cardiovascular problems, and the like, which are clearly “side” effects of the antiretroviral drugs. By refusing to acknowledge this, however, a recent article interprets the data as calling for administering these drugs to even more people, people whose immune systems are even healthier by the official criterion of CD4 counts in the blood. Under the current guidelines, treatment is recommended for asymptomatic HIV-positive people who have never had an AIDS illness at CD4 counts <200, and it is said to be optional between 200 and 350. Now, it is suggested, treatment should perhaps be recommended at counts even higher than 350:

“Reductions in AIDS-related morbidity and mortality following the advent of combination antiretroviral therapy have coincided with relative increases in chronic non-AIDS end-organ diseases among HIV+ patients….
Higher CD4+ counts on antiretroviral therapy are associated with lower rates of non-AIDS diseases and AIDS. These findings … motivate randomized studies to evaluate the effects of antiretroviral therapy on a broad set of clinical outcomes at CD4+ counts greater than 350 cells/µl.” (emphasis added; Baker et al., CD4+ count and risk of non-AIDS diseases following initial treatment for HIV infection, AIDS 22: 841)

That recommendation is based on the belief that antiretroviral drugs increase CD4 counts, and that higher CD4 counts are not only somehow associated with better health but actually cause better health and prognosis. That belief is not justified by much and long-accumulated data, however. It’s been known at least since the Concorde results published in 1994 that CD4 counts (in the blood) do not correlate with better clinical outcomes, and the large Antiretroviral Collaboration published in 2006 reported that HAART increased rather than decreased the incidence of adverse events (sources cited at p. 169 in The Origin, Persistence and Failings of HIV/AIDS Theory). In between there have been a range of articles pointing the same way, for example the finding that viral load and CD4 counts are not correlated:

“Presenting HIV RNA level predicts the rate of CD4 cell decline only minimally in untreated persons. Other factors, as yet undefined, likely drive CD4 cell losses in HIV infection” (Rodriguez et al., JAMA, 296 [2006] 1498-1506).

Note that the decline of CD4 counts in HIV-positive people remains to be explained and is not owing to the amount of purported virus measured supposedly by viral load.

Yet Baker et al. in their 2008 publication cite a 1997 paper for the beneficial effect of HAART in restoring CD4 counts, while neglecting to mention “immune restoration syndrome”, described already in 1999: the phenomenon in which supposedly restored immune-system function leads to death rather than health; and Baker et al. cite a 1998 paper reporting declining mortality, very few years after HAART was introduced, while ignoring the Antiretroviral Collaboration published in 2006 that found increased mortality.

Correctly cited are no fewer than 10 independent studies, published between 2002 and 2007, that found increased incidence of and death from liver, cardiovascular, and renal diseases, and from some cancers, among HIV-positive people on antiretroviral treatment. In their own study, remarkably, Baker et al. want to ascribe this to “prolonged survival” achieved by antiretroviral treatment. Yet the median ages of their patients who suffered or died from these non-AIDS illnesses was between 40 and 44, ages at which one does not normally expect a noticeable rate of death from cancer, or from liver or heart “end-organ” failure. Those conditions are typical effects of drugs.

Not only does the selective citation of data and the manner of interpretation adopted by Baker et al. allow much room for questions to be raised, so does the very manner in which they report the data. Here is their summary (their Table 1; “FIRST” is an acronym for the Flexible Initial Retrovirus Suppressive Therapies trial):

Please look at the numbers carefully. 188 total deaths are reported, of which 89 are from AIDS and 27 from non-AIDS “events”. “AIDS” and “non-AIDS”, one might imagine, are mutually exclusive categories that together cover all possibilities; yet 188 minus 89 minus 27 leaves 72 deaths unaccounted for.

Only several paragraphs below the table are these referred to: “16 were a result of sepsis/shock, 17 from respiratory failure or pneumonia, 17 from other cardiovascular causes (arrhythmia, heart failure, pulmonary embolus, or aneurysm), and 20 were due to unknown causes”.

How are these 17 cardiovascular-caused deaths different from the 5 reported in the Table as “non-AIDS cardiovascular”, since apparently they are not “AIDS”?

Why were not all those 72 deaths acknowledged as “non-AIDS”?

What possible reason is there not to regard these deaths as plausibly occasioned by the antiretroviral drugs?

Furthermore, what is one to say about a study in which 20 deaths — 20 out of 188, a little over 15% — are attributed to unknown causes? Who was in charge here? How were the patients being monitored? Who signed the death certificates? Why were no autopsies performed in cases of doubt about the cause of death? In a study specifically aimed at elucidating ways of decreasing mortality, what possible excuse is there for such lapses? (And, not by the way, what does this say about the quality of the editorial review and refereeing practices of this journal?)

Enough of rhetorical questions: There were actually 99 non-AIDS deaths and 89 AIDS deaths. All the causes of the non-AIDS deaths are conditions typically associated with “side” effects of drugs. Since the median age of the patients was about 40, it is more than plausible that they were caused by the antiretroviral drugs. Indeed, the latest version of the official Treatment Guidelines states (at p. 13):

“In the era of combination antiretroviral therapy, several large observational studies have indicated that the risk of several non-AIDS-defining conditions, including cardiovascular diseases, liver-related events, renal disease, and certain non-AIDS malignancies … is greater than the risk for AIDS 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.”

When there are more deaths from scenario A than from scenario B, one might prefer the latter. In other words, better NOT to use antiretroviral treatment, especially with people who initially present with no symptoms of illness and who are treated only because of laboratory tests (“HIV” and CD4) of doubtful validity and significance.

But even accepting the article’s basic premises, note that there is mention of only a correlation between CD4 counts and risk. Anyone should feel free to interpret all this differently, namely: People with higher CD4 counts (in the blood) are better prepared to stave off physiological insults than those with lower counts, and they are therefore better able to resist the toxic effects of antiretroviral drugs. Apparently, the higher one’s CD4 count, the longer one is likely to survive HAART. Recall Julianne Sacher’s explanation of why CD4 counts in the blood vary dramatically from time to time: these cells move to those parts of the body that are under attack (AIDS AS INTESTINAL DYSBIOSIS, 23 February 2008; ALTERNATIVE TREATMENTS FOR AIDS, 25 February 2008).

Baker et al., however, choose to sum up their findings thus:
“Serious non-AIDS diseases, such as liver, cardiovascular, renal, and non-AIDS cancers, have contributed significantly to morbidity and mortality among HIV-infected patients because of the introduction of potent combination ART. It is unclear to what extent this is due to chronic immunosuppression, complications of ART, coinfection, or other established risk factors . . . .
we have established an association between latest CD4+ levels and risk for end-organ diseases not attributable to AIDS following initiation of ART. Further research is needed to establish whether HIV-related immune depletion truly leads to more frequent non-AIDS diseases, and to examine the underlying mechanisms.”

In my view, it is implausible to the point of perversity to suggest “chronic immunosuppression, coinfection, or other established risk factors” as possible reasons for the increased mortality in the same breath as “complications of ART”, given that all the death events are from occurrences well known to typify iatrogenic events; they are typical “side” effects of drugs.

It also seems to me highly irresponsible to suggest “further research” that involves exposing yet more and healthier people to drugs whose toxicity is beyond doubt.

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